Title:Harnessing the Power of SIRT1 and Non-coding RNAs in Vascular Disease
VOLUME: 14 ISSUE: 1
Author(s):Kenneth Maiese
Affiliation:Cellular and Molecular Signaling, Newark, NJ
Keywords:Aging, apoptosis, autophagy, biomarker, cardiovascular disease, CCN4, cyclin-dependent kinase 2 (CDK2), cyclindependent
kinase inhibitor 1 (p21), cell cycle, circular RNA, diabetes mellitus, endothelial cells, forkhead transcription factors,
FoxO, metabolism, microRNA, non-coding RNA, oxidative stress, programmed cell death, senescence, SIRT1, stem cells, transcription
factors, WISP1, Wnt signaling.
Abstract:Noncommunicable diseases (NCDs) contribute to a significant amount of disability and death
in the world. Of these disorders, vascular disease is ranked high, falls within the five leading causes of
death, and impacts multiple other disease entities such as those of the cardiac system, nervous system, and
metabolic disease. Targeting the silent mating type information regulation 2 homolog 1 (Saccharomyces
cerevisiae) (SIRT1) pathway and the modulation of micro ribonucleic acids (miRNAs) may hold great
promise for the development of novel strategies for the treatment of vascular disease since each of these
pathways are highly relevant to cardiac and nervous system disorders as well as to metabolic dysfunction.
SIRT1 is vital in determining the course of stem cell development and the survival, metabolism, and life
span of differentiated cells that are overseen by both autophagy and apoptosis. SIRT1 interfaces with a
number of pathways that involve forkhead transcription factors, mechanistic of rapamycin (mTOR), AMP
activated protein kinase (AMPK) and Wnt1 inducible signaling pathway protein 1 (WISP1) such that the
level of activity of SIRT1 can become a critical determinant for biological and clinical outcomes. The
essential fine control of SIRT1 is directly tied to the world of non-coding RNAs that ultimately oversee
SIRT1 activity to either extend or end cellular survival. Future studies that can further elucidate the
crosstalk between SIRT1 and non-coding RNAs should serve well our ability to harness the power of
SIRT1 and non-coding RNAs for the treatment of vascular disorders.
