Abstract
Autophagy is a bulk cytosolic degradative process which in the last few years has become a key pathway for the advancement of molecular medicine. Autophagy (cellular self-eating) has several implications in human disorders involving accumulation of cytosolic protein aggregates such as Alzheimer, Parkinson, Huntington diseases, as well as in myopathies caused by deficient lysosomal functions and in cancer. Moreover, autophagy affects intracellular microorganism lifespan, acting either as a cellular defense mechanism or, on the contrary, promoting pathogen replication. Furthermore, autophagy also participates in antigen presentation, as a part of the adaptive immune response. Therefore, autophagy association with cell survival or cell death would depend on cell nutrition conditions, presence of cell intruders, and alterations in oncogene or suppressor gene expression. In this review we will focus on the wide spectra of disease-related topics where autophagy is involved, particularly, in those processes concerning microorganism infections.
Keywords: human diseases, Atg, LC3, Autophagosome
Current Molecular Medicine
Title: Autophagy: For Better or for Worse, in Good Times or in Bad Times …
Volume: 8 Issue: 2
Author(s): Sebastian D. Calligaris, Cecilia Lerena and Maria Isabel Colombo
Affiliation:
Keywords: human diseases, Atg, LC3, Autophagosome
Abstract: Autophagy is a bulk cytosolic degradative process which in the last few years has become a key pathway for the advancement of molecular medicine. Autophagy (cellular self-eating) has several implications in human disorders involving accumulation of cytosolic protein aggregates such as Alzheimer, Parkinson, Huntington diseases, as well as in myopathies caused by deficient lysosomal functions and in cancer. Moreover, autophagy affects intracellular microorganism lifespan, acting either as a cellular defense mechanism or, on the contrary, promoting pathogen replication. Furthermore, autophagy also participates in antigen presentation, as a part of the adaptive immune response. Therefore, autophagy association with cell survival or cell death would depend on cell nutrition conditions, presence of cell intruders, and alterations in oncogene or suppressor gene expression. In this review we will focus on the wide spectra of disease-related topics where autophagy is involved, particularly, in those processes concerning microorganism infections.
Export Options
About this article
Cite this article as:
Calligaris D. Sebastian, Lerena Cecilia and Colombo Isabel Maria, Autophagy: For Better or for Worse, in Good Times or in Bad Times …, Current Molecular Medicine 2008; 8 (2) . https://dx.doi.org/10.2174/156652408783769634
DOI https://dx.doi.org/10.2174/156652408783769634 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Advanced Glycation and ROS: A Link between Diabetes and Heart Failure
Current Vascular Pharmacology Remdesivir and Hydroxychloroquine: A Compassionate Use in Covid-19
Current Drug Targets Endothelial Dysfunction in Heart Failure: Mechanisms and Therapeutic Approaches
Current Vascular Pharmacology Cocaine Dependence and Stroke: Pathogenesis and Management
Current Neurovascular Research A Palliative Care Approach to the Advanced Heart Failure Patient
Current Cardiology Reviews Measurement of Physical Changes in the Myocardium for Development of Novel Methods for Diagnosing Ischemia
Current Cardiology Reviews Hypertensive Left Ventricular Hypertrophy Regression: Does It Matter?
Current Hypertension Reviews Vitamin D/VDR in Acute Kidney Injury: A Potential Therapeutic Target
Current Medicinal Chemistry MicroRNA-208a Potentiates Angiotensin II-triggered Cardiac Myoblasts Apoptosis via Inhibiting Nemo-like Kinase (NLK)
Current Pharmaceutical Design Atrial Conduction Disorders
Current Cardiology Reviews Beta-adrenergic Signaling: Complexities and Therapeutic Relevance to Heart Failure
Current Signal Transduction Therapy Dynamics of Toll-like Receptors Signaling in Skeletal Muscle Atrophy
Current Medicinal Chemistry Editorial [Hot Topic:Metabolic Therapy: An Important Therapeutic Option for the Treatment of Cardiovascular Diseases (Executive Editors: G.M.C. Rosano and G. Barbaro)]
Current Pharmaceutical Design How to Make a Non-Antigenic Protein (Auto) Antigenic: Molecular Complementarity Alters Antigen Processing and Activates Adaptive-Innate Immunity Synergy
Anti-Cancer Agents in Medicinal Chemistry Antineoplastic Chemotherapy Induced QTc Prolongation
Current Drug Safety Targeting SUMOylation Cascade for Diabetes Management
Current Drug Targets Non-Alcoholic Steatohepatitis: What Can We Learn from Animal Models?
Current Medicinal Chemistry Acute Physical Stress Increases Serum Levels of Specific microRNAs
MicroRNA Cancer Treatment-Induced Cardiotoxicity: a Cardiac Stem Cell Disease?
Cardiovascular & Hematological Agents in Medicinal Chemistry Dasatinib: An Anti-Tumour Agent via Src Inhibition
Current Drug Targets