Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Review Article

Do Mitochondrial DNA Mutations Play a Key Role in the Chronification of Sterile Inflammation? Special Focus on Atherosclerosis

Author(s): Alexander N. Orekhov*, Elena V. Gerasimova, Vasily N. Sukhorukov, Anastasia V. Poznyak* and Nikita G. Nikiforov

Volume 27 , Issue 2 , 2021

Published on: 12 October, 2020

Page: [276 - 292] Pages: 17

DOI: 10.2174/1381612826666201012164330

Price: $65

Abstract

Background: The aim of the elucidation of mechanisms implicated in the chronification of inflammation is to shed light on the pathogenesis of disorders that are responsible for the majority of the incidences of diseases and deaths, and also causes of ageing. Atherosclerosis is an example of the most significant inflammatory pathology. The inflammatory response of innate immunity is implicated in the development of atherosclerosis arising locally or focally.

Modified low-density lipoprotein (LDL) was regarded as the trigger for this response. No atherosclerotic changes in the arterial wall occur due to the quick decrease in inflammation rate. Nonetheless, the atherosclerotic lesion formation can be a result of the chronification of local inflammation, which, in turn, is caused by alteration of the response of innate immunity.

Objective: In this review, we discussed potential mechanisms of the altered response of the immunity in atherosclerosis with a particular emphasis on mitochondrial dysfunctions.

Conclusion: A few mitochondrial dysfunctions can be caused by the mitochondrial DNA (mtDNA) mutations. Moreover, mtDNA mutations were found to affect the development of defective mitophagy. Modern investigations have demonstrated the controlling mitophagy function in response to the immune system. Therefore, we hypothesized that impaired mitophagy, as a consequence of mutations in mtDNA, can raise a disturbed innate immunity response, resulting in the chronification of inflammation in atherosclerosis.

Keywords: Atherosclerosis, chronification of inflammation, defective mitophagy, innate immunity, mitochondrial dysfunction, modified LDL.

[1]
Taubert KA. Cardiology patient pages. Can patients with cardiovascular disease take nonsteroidal antiinflammatory drugs? Circulation 2008; 117(17): e322-4.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.107.749135] [PMID: 18443243]
[2]
Kirkby NS, Lundberg MH, Wright WR, Warner TD, Paul-Clark MJ, Mitchell JA. COX-2 protects against atherosclerosis independently of local vascular prostacyclin: identification of COX-2 associated pathways implicate Rgl1 and lymphocyte networks. PLoS One 2014; 9(6)e98165
[http://dx.doi.org/10.1371/journal.pone.0098165] [PMID: 24887395]
[3]
Fava C, Montagnana M. Atherosclerosis Is an Inflammatory Disease which Lacks a Common Anti-inflammatory Therapy: How Human Genetics Can Help to This Issue. A Narrative Review. Front Pharmacol 2018; 9: 55.
[http://dx.doi.org/10.3389/fphar.2018.00055] [PMID: 29467655]
[4]
Schwartz SM, Galis ZS, Rosenfeld ME, Falk E. Plaque rupture in humans and mice. Arterioscler Thromb Vasc Biol 2007; 27(4): 705-13.
[http://dx.doi.org/10.1161/01.ATV.0000261709.34878.20] [PMID: 17332493]
[5]
Aliev G, Castellani RJ, Petersen RB, Burnstock G, Perry G, Smith MA. Pathobiology of familial hypercholesterolemic atherosclerosis. J Submicrosc Cytol Pathol 2004; 36(3-4): 225-40.
[PMID: 15906597]
[6]
Sijbrands EJ. Xanthomas and atheromas. Atherosclerosis 2017; 263: 315.
[http://dx.doi.org/10.1016/j.atherosclerosis.2017.06.003] [PMID: 28606368]
[7]
Madjid M, Naghavi M, Malik BA, Litovsky S, Willerson JT, Casscells W. Thermal detection of vulnerable plaque. Am J Cardiol 2002; 90(10C): 36L-9L.
[http://dx.doi.org/10.1016/S0002-9149(02)02962-4] [PMID: 12459426]
[8]
Stary HC, Chandler AB, Dinsmore RE, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1995; 92(5): 1355-74.
[http://dx.doi.org/10.1161/01.CIR.92.5.1355] [PMID: 7648691]
[9]
Orekhov AN, Nikiforov NN, Ivanova EA, Sobenin IA. Possible Role of mitochondrial DNA mutations in chronification of inflammation: Focus on atherosclerosis. J Clin Med 2020; 9(4)E978
[http://dx.doi.org/10.3390/jcm9040978] [PMID: 32244740]
[10]
Hansson GK, Jonasson L, Lojsthed B, Stemme S, Kocher O, Gabbiani G. Localization of T lymphocytes and macrophages in fibrous and complicated human atherosclerotic plaques. Atherosclerosis 1988; 72(2-3): 135-41.
[http://dx.doi.org/10.1016/0021-9150(88)90074-3] [PMID: 3063267]
[11]
Libby P, Buring JE, Badimon L, et al. Atherosclerosis. Nat Rev Dis Primers 2019; 5(1): 56.
[http://dx.doi.org/10.1038/s41572-019-0106-z] [PMID: 31420554]
[12]
Gisterå A, Hansson GK. The immunology of atherosclerosis. Nat Rev Nephrol 13(6): 368-80.
[http://dx.doi.org/10.1038/nrneph.2017.51]
[13]
Rajendran P, Rengarajan T, Thangavel J, et al. The vascular endothelium and human diseases. Int J Biol Sci 2013; 9(10): 1057-69.
[http://dx.doi.org/10.7150/ijbs.7502] [PMID: 24250251]
[14]
Romanov YA, Balyasnikova IV, Bystrevskaya VB, et al. Endothelial heterogeneity and intimal blood-borne cells. Relation to human atherosclerosis. Ann N Y Acad Sci 1995; 748: 12-37.
[http://dx.doi.org/10.1111/j.1749-6632.1994.tb17306.x] [PMID: 7535024]
[15]
Ivanova EA, Orekhov AN. Cellular Model of Atherogenesis Based on Pluripotent Vascular Wall Pericytes. Stem Cells Int 2016.20167321404
[http://dx.doi.org/10.1155/2016/7321404] [PMID: 26880986]
[16]
Velican D, Velican C. Histochemical study on the glycosaminoglycans (acid mucopolysaccharides) of the human coronary arteries. Acta Histochem 1977; 59(2): 190-200.
[http://dx.doi.org/10.1016/S0065-1281(77)80039-1] [PMID: 412386]
[17]
Rekhter MD, Andreeva ER, Mironov AA, Orekhov AN. Three-dimensional cytoarchitecture of normal and atherosclerotic intima of human aorta. Am J Pathol 1991; 138(3): 569-80.
[PMID: 2000936]
[18]
Ivanova EA, Bobryshev YV, Orekhov AN. Intimal pericytes as the second line of immune defence in atherosclerosis. World J Cardiol 2015; 7(10): 583-93.
[http://dx.doi.org/10.4330/wjc.v7.i10.583] [PMID: 26516412]
[19]
Summerhill V, Orekhov A. Pericytes in Atherosclerosis. Adv Exp Med Biol 2019; 1147: 279-97.
[http://dx.doi.org/10.1007/978-3-030-16908-4_13] [PMID: 31147883]
[20]
Orekhov AN, Bobryshev YV, Chistiakov DA. The complexity of cell composition of the intima of large arteries: focus on pericyte-like cells. Cardiovasc Res 2014; 103(4): 438-51.
[http://dx.doi.org/10.1093/cvr/cvu168] [PMID: 25016615]
[21]
Geer JC, Haust MD. Smooth muscle cells in atherosclerosis. Monogr Atheroscler 1972; 2(0): 1-140.
[PMID: 4600684]
[22]
Summerhill VI, Grechko AV, Yet SF, Sobenin IA, Orekhov AN. The Atherogenic Role of Circulating Modified Lipids in Atherosclerosis. Int J Mol Sci 2019; 20(14)E3561
[http://dx.doi.org/10.3390/ijms20143561] [PMID: 31330845]
[23]
Orekhov AN, Sobenin IA. Modified lipoproteins as biomarkers of atherosclerosis. Front Biosci 2018; 23: 1422-44.
[http://dx.doi.org/10.2741/4653] [PMID: 29293443]
[24]
Orekhov AN, Sobenin IA. Modified and Dysfunctional Lipoproteins in Atherosclerosis: Effectors or Biomarkers? Curr Med Chem 2019; 26(9): 1512-24.
[http://dx.doi.org/10.2174/0929867325666180320121137] [PMID: 29557739]
[25]
Goldstein JL, Brown MS. The LDL receptor. Arterioscler Thromb Vasc Biol 2009; 29(4): 431-8.
[http://dx.doi.org/10.1161/ATVBAHA.108.179564] [PMID: 19299327]
[26]
Kontush A. HDL particle number and size as predictors of cardiovascular disease. Front Pharmacol 2015; 6: 218.
[http://dx.doi.org/10.3389/fphar.2015.00218] [PMID: 26500551]
[27]
Reiss AB, Patel CA, Rahman MM, et al. Interferon-gamma impedes reverse cholesterol transport and promotes foam cell transformation in THP-1 human monocytes/macrophages. Med Sci Monit 2004; 10(11): BR420-5.
[PMID: 15507847]
[28]
Hashizume M, Mihara M. Atherogenic effects of TNF-α and IL-6 via up-regulation of scavenger receptors. Cytokine 2012; 58(3): 424-30.
[http://dx.doi.org/10.1016/j.cyto.2012.02.010] [PMID: 22436638]
[29]
Xu Z, Dong A, Feng Z, Li J. Interleukin-32 promotes lipid accumulation through inhibition of cholesterol efflux. Exp Ther Med 2017; 14(2): 947-52.
[http://dx.doi.org/10.3892/etm.2017.4596] [PMID: 28781617]
[30]
Liu Q, Fan J, Bai J, et al. IL-34 promotes foam cell formation by enhancing CD36 expression through p38 MAPK pathway. Sci Rep 2018; 8(1): 17347.
[http://dx.doi.org/10.1038/s41598-018-35485-2] [PMID: 30478377]
[31]
Poznyak AV, Wu WK, Melnichenko AA, et al. Signaling Pathways and Key Genes Involved in Regulation of foam Cell Formation in Atherosclerosis. Cells 2020; 9(3)E584
[http://dx.doi.org/10.3390/cells9030584] [PMID: 32121535]
[32]
Orekhov AN, Andreeva ER, Bobryshev YV. Cellular mechanisms of human atherosclerosis: Role of cell-to-cell communications in subendothelial cell functions. Tissue Cell 2016; 48(1): 25-34.
[http://dx.doi.org/10.1016/j.tice.2015.11.002] [PMID: 26747411]
[33]
Orekhov AN, Tertov VV, Kudryashov SA, Smirnov VN. Triggerlike stimulation of cholesterol accumulation and DNA and extracellular matrix synthesis induced by atherogenic serum or low density lipoprotein in cultured cells. Circ Res 1990; 66(2): 311-20.
[http://dx.doi.org/10.1161/01.RES.66.2.311] [PMID: 2297806]
[34]
Orekhov AN, Ivanova EA. Cellular models of atherosclerosis and their implication for testing natural substances with anti-atherosclerotic potential. Phytomedicine 2016; 23(11): 1190-7.
[http://dx.doi.org/10.1016/j.phymed.2016.01.003] [PMID: 26922038]
[35]
Ishii KJ, Koyama S, Nakagawa A, Coban C, Akira S. Host innate immune receptors and beyond: making sense of microbial infections. Cell Host Microbe 2008; 3(6): 352-63.
[http://dx.doi.org/10.1016/j.chom.2008.05.003] [PMID: 18541212]
[36]
Silva MT. Macrophage phagocytosis of neutrophils at inflammatory/infectious foci: a cooperative mechanism in the control of infection and infectious inflammation. J Leukoc Biol 2011; 89(5): 675-83.
[http://dx.doi.org/10.1189/jlb.0910536] [PMID: 21169518]
[37]
Kawai T, Akira S. Toll-like receptors and their crosstalk with other innate receptors in infection and immunity. Immunity 2011; 34(5): 637-50.
[http://dx.doi.org/10.1016/j.immuni.2011.05.006] [PMID: 21616434]
[38]
Martinon F, Mayor A, Tschopp J. The inflammasomes: guardians of the body. Annu Rev Immunol 2009; 27: 229-65.
[http://dx.doi.org/10.1146/annurev.immunol.021908.132715] [PMID: 19302040]
[39]
Yang K, Wang X, Liu Z, et al. Oxidized low-density lipoprotein promotes macrophage lipid accumulation via the toll-like receptor 4-Src pathway. Circ J 2015; 79(11): 2509-16.
[http://dx.doi.org/10.1253/circj.CJ-15-0345] [PMID: 26399924]
[40]
Wang JG, Aikawa M. Toll-like receptors and Src-family kinases in atherosclerosis - focus on macrophages. Circ J 2015; 79(11): 2332-4.
[http://dx.doi.org/10.1253/circj.CJ-15-1039] [PMID: 26467082]
[41]
Hovland A, Jonasson L, Garred P, et al. The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis. Atherosclerosis 2015; 241(2): 480-94.
[http://dx.doi.org/10.1016/j.atherosclerosis.2015.05.038] [PMID: 26086357]
[42]
Karasawa T, Takahashi M. Role of NLRP3 Inflammasomes in Atherosclerosis. J Atheroscler Thromb 2017; 24(5): 443-51.
[http://dx.doi.org/10.5551/jat.RV17001] [PMID: 28260724]
[43]
Matsuura E, Lopez LR, Shoenfeld Y, Ames PR. β2-glycoprotein I and oxidative inflammation in early atherogenesis: a progression from innate to adaptive immunity? Autoimmun Rev 2012; 12(2): 241-9.
[http://dx.doi.org/10.1016/j.autrev.2012.04.003] [PMID: 22569463]
[44]
Murray PJ, Wynn TA. Protective and pathogenic functions of macrophage subsets. Nat Rev Immunol 2011; 11(11): 723-37.
[http://dx.doi.org/10.1038/nri3073] [PMID: 21997792]
[45]
Vallabhapurapu S, Karin M. Regulation and function of NF-kappaB transcription factors in the immune system. Annu Rev Immunol 2009; 27: 693-733.
[http://dx.doi.org/10.1146/annurev.immunol.021908.132641] [PMID: 19302050]
[46]
Afonina IS, Zhong Z, Karin M, Beyaert R. Limiting inflammation-the negative regulation of NF-κB and the NLRP3 inflammasome. Nat Immunol 2017; 18(8): 861-9.
[http://dx.doi.org/10.1038/ni.3772] [PMID: 28722711]
[47]
Schroder K, Tschopp J. The inflammasomes. Cell 2010; 140(6): 821-32.
[http://dx.doi.org/10.1016/j.cell.2010.01.040] [PMID: 20303873]
[48]
Guo H, Callaway JB, Ting JP. Inflammasomes: mechanism of action, role in disease, and therapeutics. Nat Med 2015; 21(7): 677-87.
[http://dx.doi.org/10.1038/nm.3893] [PMID: 26121197]
[49]
Strowig T, Henao-Mejia J, Elinav E, Flavell R. Inflammasomes in health and disease. Nature 2012; 481(7381): 278-86.
[http://dx.doi.org/10.1038/nature10759] [PMID: 22258606]
[50]
Davis BK, Wen H, Ting JP. The inflammasome NLRs in immunity, inflammation, and associated diseases. Annu Rev Immunol 2011; 29: 707-35.
[http://dx.doi.org/10.1146/annurev-immunol-031210-101405] [PMID: 21219188]
[51]
de Zoete MR, Palm NW, Zhu S, Flavell RA. Inflammasomes. Cold Spring Harb Perspect Biol 2014; 6(12)a016287
[http://dx.doi.org/10.1101/cshperspect.a016287] [PMID: 25324215]
[52]
Liu Q, Zhang D, Hu D, Zhou X, Zhou Y. The role of mitochondria in NLRP3 inflammasome activation. Mol Immunol 2018; 103: 115-24.
[http://dx.doi.org/10.1016/j.molimm.2018.09.010] [PMID: 30248487]
[53]
Hoseini Z, Sepahvand F, Rashidi B, Sahebkar A, Masoudifar A, Mirzaei H. NLRP3 inflammasome: Its regulation and involvement in atherosclerosis. J Cell Physiol 2018; 233(3): 2116-32.
[http://dx.doi.org/10.1002/jcp.25930] [PMID: 28345767]
[54]
Gurung P, Lukens JR, Kanneganti TD. Mitochondria: diversity in the regulation of the NLRP3 inflammasome. Trends Mol Med 2015; 21(3): 193-201.
[http://dx.doi.org/10.1016/j.molmed.2014.11.008] [PMID: 25500014]
[55]
Mills EL, Kelly B, O’Neill LAJ. Mitochondria are the powerhouses of immunity. Nat Immunol 2017; 18(5): 488-98.
[http://dx.doi.org/10.1038/ni.3704] [PMID: 28418387]
[56]
Tschopp J. Mitochondria: Sovereign of inflammation? Eur J Immunol 2011; 41(5): 1196-202.
[http://dx.doi.org/10.1002/eji.201141436] [PMID: 21469137]
[57]
Kim YG, Kim SM, Kim KP, Lee SH, Moon JY. The Role of Inflammasome-Dependent and Inflammasome-Independent NLRP3 in the Kidney. Cells 2019; 8(11)E1389
[http://dx.doi.org/10.3390/cells8111389] [PMID: 31694192]
[58]
Vaamonde-García C, López-Armada MJ. Role of mitochondrial dysfunction on rheumatic diseases. Biochem Pharmacol 2019; 165: 181-95.
[http://dx.doi.org/10.1016/j.bcp.2019.03.008] [PMID: 30862506]
[59]
Wang Z, Wu M. Phylogenomic reconstruction indicates mitochondrial ancestor was an energy parasite. PLoS One 2014; 9(10)e110685
[http://dx.doi.org/10.1371/journal.pone.0110685] [PMID: 25333787]
[60]
Archibald JM. Endosymbiosis and Eukaryotic Cell Evolution. Curr Biol 2015; 25(19): R911-21.
[http://dx.doi.org/10.1016/j.cub.2015.07.055] [PMID: 26439354]
[61]
Twig G, Hyde B, Shirihai OS. Mitochondrial fusion, fission and autophagy as a quality control axis: the bioenergetic view. Biochim Biophys Acta 2008; 1777(9): 1092-7.
[http://dx.doi.org/10.1016/j.bbabio.2008.05.001] [PMID: 18519024]
[62]
Osman C, Voelker DR, Langer T. Making heads or tails of phospholipids in mitochondria. J Cell Biol 2011; 192(1): 7-16.
[http://dx.doi.org/10.1083/jcb.201006159] [PMID: 21220505]
[63]
Zhang Q, Raoof M, Chen Y, et al. Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature 2010; 464(7285): 104-7.
[http://dx.doi.org/10.1038/nature08780] [PMID: 20203610]
[64]
Krysko DV, Agostinis P, Krysko O, et al. Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation. Trends Immunol 2011; 32(4): 157-64.
[http://dx.doi.org/10.1016/j.it.2011.01.005] [PMID: 21334975]
[65]
Ghayur T, Banerjee S, Hugunin M, et al. Caspase-1 processes IFN-gamma-inducing factor and regulates LPS-induced IFN-gamma production. Nature 1997; 386(6625): 619-23.
[http://dx.doi.org/10.1038/386619a0] [PMID: 9121587]
[66]
Iyer SS, He Q, Janczy JR, et al. Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation. Immunity 2013; 39(2): 311-23.
[http://dx.doi.org/10.1016/j.immuni.2013.08.001] [PMID: 23954133]
[67]
Yu J, Nagasu H, Murakami T, et al. Inflammasome activation leads to Caspase-1-dependent mitochondrial damage and block of mitophagy. Proc Natl Acad Sci USA 2014; 111(43): 15514-9.
[http://dx.doi.org/10.1073/pnas.1414859111] [PMID: 25313054]
[68]
Fischer F, Hamann A, Osiewacz HD. Mitochondrial quality control: an integrated network of pathways. Trends Biochem Sci 2012; 37(7): 284-92.
[http://dx.doi.org/10.1016/j.tibs.2012.02.004] [PMID: 22410198]
[69]
Szklarczyk R, Nooteboom M, Osiewacz HD. Control of mitochondrial integrity in ageing and disease Philos Trans R Soc Lond B Biol Sci 2014; 369(1646) 0439.
[http://dx.doi.org/10.1098/rstb.2013.0439] [PMID: 24864310]
[70]
Tan T, Zimmermann M, Reichert AS. Controlling quality and amount of mitochondria by mitophagy: insights into the role of ubiquitination and deubiquitination. Biol Chem 2016; 397(7): 637-47.
[http://dx.doi.org/10.1515/hsz-2016-0125] [PMID: 27145142]
[71]
Zhong Z, Umemura A, Sanchez-Lopez E, et al. NF-κB Restricts Inflammasome Activation via Elimination of Damaged Mitochondria. Cell 2016; 164(5): 896-910.
[http://dx.doi.org/10.1016/j.cell.2015.12.057] [PMID: 26919428]
[72]
Madamanchi NR, Runge MS. Mitochondrial dysfunction in atherosclerosis. Circ Res 2007; 100(4): 460-73.
[http://dx.doi.org/10.1161/01.RES.0000258450.44413.96] [PMID: 17332437]
[73]
Peng W, Cai G, Xia Y, et al. Mitochondrial Dysfunction in Atherosclerosis. DNA Cell Biol 2019; 38(7): 597-606.
[http://dx.doi.org/10.1089/dna.2018.4552] [PMID: 31095428]
[74]
Chistiakov DA, Shkurat TP, Melnichenko AA, Grechko AV, Orekhov AN. The role of mitochondrial dysfunction in cardiovascular disease: a brief review. Ann Med 2018; 50(2): 121-7.
[http://dx.doi.org/10.1080/07853890.2017.1417631] [PMID: 29237304]
[75]
Foote K, Reinhold J, Yu EPK, et al. Restoring mitochondrial DNA copy number preserves mitochondrial function and delays vascular aging in mice. Aging Cell 2018; 17(4)e12773
[http://dx.doi.org/10.1111/acel.12773] [PMID: 29745022]
[76]
Shalapour S, Karin M. Immunity, inflammation, and cancer: an eternal fight between good and evil. J Clin Invest 2015; 125(9): 3347-55.
[http://dx.doi.org/10.1172/JCI80007] [PMID: 26325032]
[77]
Nishino M, Ramaiya NH, Hatabu H, Hodi FS. Monitoring immune-checkpoint blockade: response evaluation and biomarker development. Nat Rev Clin Oncol 2017; 14(11): 655-68.
[http://dx.doi.org/10.1038/nrclinonc.2017.88] [PMID: 28653677]
[78]
Lee HC, Yin PH, Lin JC, et al. Mitochondrial genome instability and mtDNA depletion in human cancers. Ann N Y Acad Sci 2005; 1042: 109-22.
[http://dx.doi.org/10.1196/annals.1338.011] [PMID: 15965052]
[79]
Petros JA, Baumann AK, Ruiz-Pesini E, et al. mtDNA mutations increase tumorigenicity in prostate cancer. Proc Natl Acad Sci USA 2005; 102(3): 719-24.
[http://dx.doi.org/10.1073/pnas.0408894102] [PMID: 15647368]
[80]
Shidara Y, Yamagata K, Kanamori T, et al. Positive contribution of pathogenic mutations in the mitochondrial genome to the promotion of cancer by prevention from apoptosis. Cancer Res 2005; 65(5): 1655-63.
[http://dx.doi.org/10.1158/0008-5472.CAN-04-2012] [PMID: 15753359]
[81]
Higuchi M, Kudo T, Suzuki S, et al. Mitochondrial DNA determines androgen dependence in prostate cancer cell lines. Oncogene 2006; 25(10): 1437-45.
[http://dx.doi.org/10.1038/sj.onc.1209190] [PMID: 16278679]
[82]
Ishikawa K, Takenaga K, Akimoto M, et al. ROS-generating mitochondrial DNA mutations can regulate tumor cell metastasis. Science 2008; 320(5876): 661-4.
[http://dx.doi.org/10.1126/science.1156906] [PMID: 18388260]
[83]
Singh KK, Ayyasamy V, Owens KM, Koul MS, Vujcic M. Mutations in mitochondrial DNA polymerase-gamma promote breast tumorigenesis. J Hum Genet 2009; 54(9): 516-24.
[http://dx.doi.org/10.1038/jhg.2009.71] [PMID: 19629138]
[84]
Kang MJ, Shadel GS. A Mitochondrial Perspective of Chronic Obstructive Pulmonary Disease Pathogenesis. Tuberc Respir Dis (Seoul) 2016; 79(4): 207-13.
[http://dx.doi.org/10.4046/trd.2016.79.4.207] [PMID: 27790272]
[85]
Kang MJ, Yoon CM, Kim BH, et al. Suppression of NLRX1 in chronic obstructive pulmonary disease. J Clin Invest 2015; 125(6): 2458-62.
[http://dx.doi.org/10.1172/JCI71747] [PMID: 25938787]
[86]
Yoon CM, Nam M, Oh YM, Dela Cruz CS, Kang MJ. Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease. J Innate Immun 2016; 8(2): 121-8.
[http://dx.doi.org/10.1159/000441299] [PMID: 26536345]
[87]
Puente-Maestu L, Lázaro A, Tejedor A, et al. Effects of exercise on mitochondrial DNA content in skeletal muscle of patients with COPD. Thorax 2011; 66(2): 121-7.
[http://dx.doi.org/10.1136/thx.2010.153031] [PMID: 21097816]
[88]
Puente-Maestu L, Pérez-Parra J, Godoy R, et al. Abnormal mitochondrial function in locomotor and respiratory muscles of COPD patients. Eur Respir J 2009; 33(5): 1045-52.
[http://dx.doi.org/10.1183/09031936.00112408] [PMID: 19129279]
[89]
Rabinovich RA, Bastos R, Ardite E, et al. Mitochondrial dysfunction in COPD patients with low body mass index. Eur Respir J 2007; 29(4): 643-50.
[http://dx.doi.org/10.1183/09031936.00086306] [PMID: 17182653]
[90]
Zhang X, Shan P, Homer R, et al. Cathepsin E promotes pulmonary emphysema via mitochondrial fission. Am J Pathol 2014; 184(10): 2730-41.
[http://dx.doi.org/10.1016/j.ajpath.2014.06.017] [PMID: 25239563]
[91]
Bewley MA, Preston JA, Mohasin M, et al. Impaired Mitochondrial Microbicidal Responses in Chronic Obstructive Pulmonary Disease Macrophages. Am J Respir Crit Care Med 2017; 196(7): 845-55.
[http://dx.doi.org/10.1164/rccm.201608-1714OC] [PMID: 28557543]
[92]
Mora AL, Bueno M, Rojas M. Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis. J Clin Invest 2017; 127(2): 405-14.
[http://dx.doi.org/10.1172/JCI87440] [PMID: 28145905]
[93]
Dromparis P, Michelakis ED. Mitochondria in vascular health and disease. Annu Rev Physiol 2013; 75: 95-126.
[http://dx.doi.org/10.1146/annurev-physiol-030212-183804] [PMID: 23157555]
[94]
Iyer D, Mishra N, Agrawal A. Mitochondrial Function in Allergic Disease. Curr Allergy Asthma Rep 2017; 17(5): 29.
[http://dx.doi.org/10.1007/s11882-017-0695-0] [PMID: 28429306]
[95]
Valdivieso AG, Santa-Coloma TA. CFTR activity and mitochondrial function. Redox Biol 2013; 1: 190-202.
[http://dx.doi.org/10.1016/j.redox.2012.11.007] [PMID: 24024153]
[96]
Smallwood MJ, Nissim A, Knight AR, Whiteman M, Haigh R, Winyard PG. Oxidative stress in autoimmune rheumatic diseases. Free Radic Biol Med 2018; 125: 3-14.
[http://dx.doi.org/10.1016/j.freeradbiomed.2018.05.086] [PMID: 29859343]
[97]
Goris A, Liston A. The immunogenetic architecture of autoimmune disease. Cold Spring Harb Perspect Biol 2012; 4(3)
[http://dx.doi.org/10.1101/cshperspect.a007260]
[98]
Lee HT, Wu TH, Lin CS, et al. The pathogenesis of systemic lupus erythematosus - From the viewpoint of oxidative stress and mitochondrial dysfunction. Mitochondrion 2016; 30: 1-7.
[99]
Valcárcel-Ares MN, Riveiro-Naveira RR, Vaamonde-García C, et al. Mitochondrial dysfunction promotes and aggravates the inflammatory response in normal human synoviocytes. Rheumatology (Oxford) 2014; 53(7): 1332-43.
[http://dx.doi.org/10.1093/rheumatology/keu016] [PMID: 24609059]
[100]
Perl A, Hanczko R, Doherty E. Assessment of mitochondrial dysfunction in lymphocytes of patients with systemic lupus erythematosus. Methods Mol Biol 2012; 900: 61-89.
[http://dx.doi.org/10.1007/978-1-60761-720-4_4] [PMID: 22933065]
[101]
Donnelly S, Roake W, Brown S, et al. Impaired recognition of apoptotic neutrophils by the C1q/calreticulin and CD91 pathway in systemic lupus erythematosus. Arthritis Rheum 2006; 54(5): 1543-56.
[http://dx.doi.org/10.1002/art.21783] [PMID: 16645988]
[102]
Muñoz LE, Lauber K, Schiller M, Manfredi AA, Herrmann M. The role of defective clearance of apoptotic cells in systemic autoimmunity. Nat Rev Rheumatol 2010; 6(5): 280-9.
[http://dx.doi.org/10.1038/nrrheum.2010.46] [PMID: 20431553]
[103]
Mambo E, Gao X, Cohen Y, Guo Z, Talalay P, Sidransky D. Electrophile and oxidant damage of mitochondrial DNA leading to rapid evolution of homoplasmic mutations. Proc Natl Acad Sci USA 2003; 100(4): 1838-43.
[http://dx.doi.org/10.1073/pnas.0437910100] [PMID: 12578990]
[104]
Lee HT, Wu TH, Lin CS, et al. Oxidative DNA and mitochondrial DNA change in patients with SLE. Front Biosci 2017; 22(22): 493-503.
[PMID: 27814627]
[105]
Kauppila TES, Kauppila JHK, Larsson NG. Mammalian Mitochondria and Aging: An Update. Cell Metab 2017; 25(1): 57-71.
[http://dx.doi.org/10.1016/j.cmet.2016.09.017] [PMID: 28094012]
[106]
Franceschi C, Bonafè M, Valensin S, et al. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci 2000; 908: 244-54.
[http://dx.doi.org/10.1111/j.1749-6632.2000.tb06651.x] [PMID: 10911963]
[107]
Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci 2014; 69(Suppl. 1): S4-9.
[http://dx.doi.org/10.1093/gerona/glu057] [PMID: 24833586]
[108]
Salminen A, Kaarniranta K, Kauppinen A. Inflammaging: disturbed interplay between autophagy and inflammasomes. Aging (Albany NY) 2012; 4(3): 166-75.
[http://dx.doi.org/10.18632/aging.100444] [PMID: 22411934]
[109]
Fivenson EM, Lautrup S, Sun N, et al. Mitophagy in neurodegeneration and aging. Neurochem Int 2017; 109: 202-9.
[http://dx.doi.org/10.1016/j.neuint.2017.02.007] [PMID: 28235551]
[110]
Lerner CA, Sundar IK, Rahman I. Mitochondrial redox system dynamics and dysfunction in lung inflammaging and COPD Int J Biochem Cell Biol 2016; 81(B): 294-306.
[http://dx.doi.org/10.1016/j.biocel.2016.07.026]
[111]
Fang EF, Scheibye-Knudsen M, Brace LE, et al. Defective mitophagy in XPA via PARP-1 hyperactivation and NAD(+)/SIRT1 reduction. Cell 2014; 157(4): 882-96.
[http://dx.doi.org/10.1016/j.cell.2014.03.026] [PMID: 24813611]
[112]
Nicholls TJ, Minczuk M. In D-loop: 40 years of mitochondrial 7S DNA. Exp Gerontol 2014; 56: 175-81.
[http://dx.doi.org/10.1016/j.exger.2014.03.027] [PMID: 24709344]
[113]
Schroeder P, Gremmel T, Berneburg M, Krutmann J. Partial depletion of mitochondrial DNA from human skin fibroblasts induces a gene expression profile reminiscent of photoaged skin. J Invest Dermatol 2008; 128(9): 2297-303.
[http://dx.doi.org/10.1038/jid.2008.57] [PMID: 18337828]
[114]
Fukui H, Moraes CT. Mechanisms of formation and accumulation of mitochondrial DNA deletions in aging neurons. Hum Mol Genet 2009; 18(6): 1028-36.
[http://dx.doi.org/10.1093/hmg/ddn437] [PMID: 19095717]
[115]
Vermulst M, Wanagat J, Kujoth GC, et al. DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice. Nat Genet 2008; 40(4): 392-4.
[http://dx.doi.org/10.1038/ng.95] [PMID: 18311139]
[116]
Larsson NG. Somatic mitochondrial DNA mutations in mammalian aging. Annu Rev Biochem 2010; 79: 683-706.
[http://dx.doi.org/10.1146/annurev-biochem-060408-093701] [PMID: 20350166]
[117]
Li H, Shen L, Hu P, et al. Aging-associated mitochondrial DNA mutations alter oxidative phosphorylation machinery and cause mitochondrial dysfunctions. Biochim Biophys Acta Mol Basis Dis 2017; 1863(9): 2266-73.
[http://dx.doi.org/10.1016/j.bbadis.2017.05.022] [PMID: 28559044]
[118]
Ding Y, Leng J, Fan F, Xia B, Xu P. The role of mitochondrial DNA mutations in hearing loss. Biochem Genet 2013; 51(7-8): 588-602.
[http://dx.doi.org/10.1007/s10528-013-9589-6] [PMID: 23605717]
[119]
Gong S, Wang X, Meng F, et al. Overexpression of mitochondrial histidyl-tRNA synthetase restores mitochondrial dysfunction caused by a deafness-associated tRNAHis mutation. J Biol Chem 2020; 295(4): 940-54.
[http://dx.doi.org/10.1074/jbc.RA119.010998] [PMID: 31819004]
[120]
Orekhov AN, Poznyak AV, Sobenin IA, Nikifirov NN, Ivanova EA. Mitochondrion as a selective target for treatment of atherosclerosis: Role of mitochondrial DNA mutations and defective mitophagy in the pathogenesis of atherosclerosis and chronic inflammation. Curr Neuropharmacol 2020; 18(11): 1064-75.
[http://dx.doi.org/10.2174/1570159X17666191118125018] [PMID: 31744449]
[121]
Sazonova MA, Sinyov VV, Ryzhkova AI, et al. Role of Mitochondrial Genome Mutations in Pathogenesis of Carotid Atherosclerosis. Oxid Med Cell Longev 2017; 20176934394
[http://dx.doi.org/10.1155/2017/6934394] [PMID: 28951770]
[122]
Sobenin IA, Zhelankin AV, Mitrofanov KY, et al. Mutations of mitochondrial DNA in atherosclerosis and atherosclerosis-related diseases. Curr Pharm Des 2015; 21(9): 1158-63.
[http://dx.doi.org/10.2174/1381612820666141013133000] [PMID: 25312735]
[123]
Sobenin IA, Sazonova MA, Postnov AY, Salonen JT, Bobryshev YV, Orekhov AN. Association of mitochondrial genetic variation with carotid atherosclerosis. PLoS One 2013; 8(7)e68070
[http://dx.doi.org/10.1371/journal.pone.0068070] [PMID: 23874496]
[124]
Andreassi MG. Coronary atherosclerosis and somatic mutations: an overview of the contributive factors for oxidative DNA damage. Mutat Res 2003; 543(1): 67-86.
[http://dx.doi.org/10.1016/S1383-5742(02)00089-3] [PMID: 12510018]
[125]
Avital G, Buchshtav M, Zhidkov I, et al. Mitochondrial DNA heteroplasmy in diabetes and normal adults: role of acquired and inherited mutational patterns in twins. Hum Mol Genet 2012; 21(19): 4214-24.
[http://dx.doi.org/10.1093/hmg/dds245] [PMID: 22736028]
[126]
Marian AJ. Mitochondrial genetics and human systemic hypertension. Circ Res 2011; 108(7): 784-6.
[http://dx.doi.org/10.1161/CIRCRESAHA.111.242768] [PMID: 21454791]
[127]
Nomiyama T, Tanaka Y, Piao L, et al. Accumulation of somatic mutation in mitochondrial DNA and atherosclerosis in diabetic patients. Ann N Y Acad Sci 2004; 1011: 193-204.
[http://dx.doi.org/10.1196/annals.1293.020] [PMID: 15126297]
[128]
Wallace DC. Colloquium paper: bioenergetics, the origins of complexity, and the ascent of man. Proc Natl Acad Sci USA 2010; 107(Suppl. 2): 8947-53.
[http://dx.doi.org/10.1073/pnas.0914635107] [PMID: 20445102]
[129]
Yu E, Foote K, Bennett M. Mitochondrial function in thoracic aortic aneurysms. Cardiovasc Res 2018; 114(13): 1696-8.
[http://dx.doi.org/10.1093/cvr/cvy180] [PMID: 29985972]
[130]
Sazonova MA, Sinyov VV, Barinova VA, et al. Mosaicism of mitochondrial genetic variation in atherosclerotic lesions of the human aorta. BioMed Res Int 2015; 2015825468
[http://dx.doi.org/10.1155/2015/825468] [PMID: 25834827]
[131]
Han CB, Ma JM, Xin Y, et al. Mutations of mitochondrial 12S rRNA in gastric carcinoma and their significance. World J Gastroenterol 2005; 11(1): 31-5.
[http://dx.doi.org/10.3748/wjg.v11.i1.31] [PMID: 15609392]
[132]
Li R, Xing G, Yan M, et al. Cosegregation of C-insertion at position 961 with the A1555G mutation of the mitochondrial 12S rRNA gene in a large Chinese family with maternally inherited hearing loss. Am J Med Genet A 2004; 124A(2): 113-7.
[http://dx.doi.org/10.1002/ajmg.a.20305] [PMID: 14699607]
[133]
Giordano C, Pallotti F, Walker WF, et al. Pathogenesis of the deafness-associated A1555G mitochondrial DNA mutation. Biochem Biophys Res Commun 2002; 293(1): 521-9.
[http://dx.doi.org/10.1016/S0006-291X(02)00256-5] [PMID: 12054632]
[134]
Bykhovskaya Y, Shohat M, Ehrenman K, et al. Evidence for complex nuclear inheritance in a pedigree with nonsyndromic deafness due to a homoplasmic mitochondrial mutation. Am J Med Genet 1998; 77(5): 421-6.
[http://dx.doi.org/10.1002/(SICI)1096-8628(19980605)77:5<421:AID-AJMG13>3.0.CO;2-K] [PMID: 9632174]
[135]
Jeppesen TD, Schwartz M, Hansen K, Danielsen ER, Wibrand F, Vissing J. Late onset of stroke-like episode associated with a 3256C->T point mutation of mitochondrial DNA. J Neurol Sci 2003; 214(1-2): 17-20.
[http://dx.doi.org/10.1016/S0022-510X(03)00168-0] [PMID: 12972383]
[136]
Matsunaga H, Tanaka Y, Tanaka M, et al. Antiatherogenic mitochondrial genotype in patients with type 2 diabetes. Diabetes Care 2001; 24(3): 500-3.
[http://dx.doi.org/10.2337/diacare.24.3.500] [PMID: 11289475]
[137]
Mukae S, Aoki S, Itoh S, et al. Mitochondrial 5178A/C genotype is associated with acute myocardial infarction. Circ J 2003; 67(1): 16-20.
[http://dx.doi.org/10.1253/circj.67.16] [PMID: 12520145]
[138]
Fu K, Hartlen R, Johns T, Genge A, Karpati G, Shoubridge EA. A novel heteroplasmic tRNAleu(CUN) mtDNA point mutation in a sporadic patient with mitochondrial encephalomyopathy segregates rapidly in skeletal muscle and suggests an approach to therapy. Hum Mol Genet 1996; 5(11): 1835-40.
[http://dx.doi.org/10.1093/hmg/5.11.1835] [PMID: 8923013]
[139]
Chol M, Lebon S, Bénit P, et al. The mitochondrial DNA G13513A MELAS mutation in the NADH dehydrogenase 5 gene is a frequent cause of Leigh-like syndrome with isolated complex I deficiency. J Med Genet 2003; 40(3): 188-91.
[http://dx.doi.org/10.1136/jmg.40.3.188] [PMID: 12624137]
[140]
Ruiter EM, Siers MH, van den Elzen C, et al. The mitochondrial 13513G > A mutation is most frequent in Leigh syndrome combined with reduced complex I activity, optic atrophy and/or Wolff-Parkinson-White. Eur J Hum Genet 2007; 15(2): 155-61.
[http://dx.doi.org/10.1038/sj.ejhg.5201735] [PMID: 17106447]
[141]
Brown MD, Voljavec AS, Lott MT, Torroni A, Yang CC, Wallace DC. Mitochondrial DNA complex I and III mutations associated with Leber’s hereditary optic neuropathy. Genetics 1992; 130(1): 163-73.
[PMID: 1732158]
[142]
Andreu AL, Bruno C, Shanske S, et al. Missense mutation in the mtDNA cytochrome b gene in a patient with myopathy. Neurology 1998; 51(5): 1444-7.
[http://dx.doi.org/10.1212/WNL.51.5.1444] [PMID: 9818877]
[143]
Sazonova M, Budnikov E, Khasanova Z, Sobenin I, Postnov A, Orekhov A. Studies of the human aortic intima by a direct quantitative assay of mutant alleles in the mitochondrial genome. Atherosclerosis 2009; 204(1): 184-90.
[http://dx.doi.org/10.1016/j.atherosclerosis.2008.09.001] [PMID: 18849029]
[144]
Orekhov AN, Zhelankin AV, Kolmychkova KI, et al. Susceptibility of monocytes to activation correlates with atherogenic mitochondrial DNA mutations. Exp Mol Pathol 2015; 99(3): 672-6.
[http://dx.doi.org/10.1016/j.yexmp.2015.11.006] [PMID: 26551079]
[145]
Dominguez-Andres J, Netea MG. Long-term reprogramming of the innate immune system. J Leukoc Biol 2019; 105(2): 329-38.
[http://dx.doi.org/10.1002/JLB.MR0318-104R] [PMID: 29999546]
[146]
Netea MG. Training innate immunity: the changing concept of immunological memory in innate host defence. Eur J Clin Invest 2013; 43(8): 881-4.
[http://dx.doi.org/10.1111/eci.12132] [PMID: 23869409]
[147]
Palikaras K, Lionaki E, Tavernarakis N. Coordination of mitophagy and mitochondrial biogenesis during ageing in C. elegans. Nature 2015; 521(7553): 525-8.
[http://dx.doi.org/10.1038/nature14300] [PMID: 25896323]
[148]
Montava-Garriga L, Ganley IG. do not know. J. Mol. Biol. 432 206-230.; Xu Y. Shen J. and Ran Z. (2019). Emerging views of mitophagy in immunity and autoimmune diseases. Autophagy 2020; 16: 3-17.
[http://dx.doi.org/10.1080/15548627.2019.1603547]
[149]
Zhang J, Ji Y, Lu Y, et al. Leber’s hereditary optic neuropathy (LHON)-associated ND5 12338T > C mutation altered the assembly and function of complex I, apoptosis and mitophagy. Hum Mol Genet 2018; 27(11): 1999-2011.
[http://dx.doi.org/10.1093/hmg/ddy107] [PMID: 29579248]
[150]
Sharma LK, Tiwari M, Rai NK, Bai Y. Mitophagy activation repairs Leber’s hereditary optic neuropathy-associated mitochondrial dysfunction and improves cell survival. Hum Mol Genet 2019; 28(3): 422-33.
[http://dx.doi.org/10.1093/hmg/ddy354] [PMID: 30304398]
[151]
Orogo AM, Gonzalez ER, Kubli DA, et al. Accumulation of Mitochondrial DNA Mutations Disrupts Cardiac Progenitor Cell Function and Reduces Survival. J Biol Chem 2015; 290(36): 22061-75.
[http://dx.doi.org/10.1074/jbc.M115.649657] [PMID: 26183775]
[152]
Granatiero V, Giorgio V, Calì T, et al. Reduced mitochondrial Ca(2+) transients stimulate autophagy in human fibroblasts carrying the 13514A>G mutation of the ND5 subunit of NADH dehydrogenase. Cell Death Differ 2016; 23(2): 231-41.
[http://dx.doi.org/10.1038/cdd.2015.84] [PMID: 26206091]
[153]
Gilkerson RW, De Vries RL, Lebot P, et al. Mitochondrial autophagy in cells with mtDNA mutations results from synergistic loss of transmembrane potential and mTORC1 inhibition. Hum Mol Genet 2012; 21(5): 978-90.
[http://dx.doi.org/10.1093/hmg/ddr529] [PMID: 22080835]
[154]
Gkikas I, Palikaras K, Tavernarakis N. The Role of Mitophagy in Innate Immunity. Front Immunol 2018; 9: 1283.
[http://dx.doi.org/10.3389/fimmu.2018.01283] [PMID: 29951054]
[155]
Lai JH, Luo SF, Ho LJ. Operation of mitochondrial machinery in viral infection-induced immune responses. Biochem Pharmacol 2018; 156: 348-56.
[http://dx.doi.org/10.1016/j.bcp.2018.08.044] [PMID: 30172712]
[156]
Rongvaux A. Innate immunity and tolerance toward mitochondria. Mitochondrion 2018; 41: 14-20.
[http://dx.doi.org/10.1016/j.mito.2017.10.007] [PMID: 29054471]
[157]
Zhang L, Qin Y, Chen M. Viral strategies for triggering and manipulating mitophagy. Autophagy 2018; 14(10): 1665-73.
[http://dx.doi.org/10.1080/15548627.2018.1466014] [PMID: 29895192]
[158]
Mohanty A, Tiwari-Pandey R, Pandey NR. Mitochondria: the indispensable players in innate immunity and guardians of the inflammatory response. J Cell Commun Signal 2019; 13(3): 303-18.
[http://dx.doi.org/10.1007/s12079-019-00507-9] [PMID: 30719617]
[159]
Cho DH, Kim JK, Jo EK. Mitophagy and Innate Immunity in Infection. Mol Cells 2020; 43(1): 10-22.
[PMID: 31999918]
[160]
Tertov VV, Sobenin IA, Gabbasov ZA, et al. Multiple-modified desialylated low density lipoproteins that cause intracellular lipid accumulation. Isolation, fractionation and characterization. Lab Invest 1992; 67(5): 665-75.
[PMID: 1434544]
[161]
Tertov VV, Sobenin IA, Gabbasov ZA, Popov EG, Orekhov AN. Lipoprotein aggregation as an essential condition of intracellular lipid accumulation caused by modified low density lipoproteins. Biochem Biophys Res Commun 1989; 163(1): 489-94.
[http://dx.doi.org/10.1016/0006-291X(89)92163-3] [PMID: 2775281]
[162]
Orekhov AN, Nikiforov NG, Elizova NV, et al. Tumor Necrosis Factor-α and C-C Motif Chemokine Ligand 18 Associate with Atherosclerotic Lipid Accumulation In situ and In vitro. Curr Pharm Des 2018; 24(24): 2883-9.
[http://dx.doi.org/10.2174/1381612824666180911120726] [PMID: 30205791]
[163]
Meyer A, Laverny G, Bernardi L, et al. Mitochondria: An Organelle of Bacterial Origin Controlling Inflammation. Front Immunol 2018; 9: 536.
[http://dx.doi.org/10.3389/fimmu.2018.00536] [PMID: 29725325]

Rights & Permissions Print Export Cite as
© 2022 Bentham Science Publishers | Privacy Policy