Abstract
The causes of aging and determinants of maximum lifespan in animal species are multifaceted and complex. However, a wealth of experimental data suggests that mitochondria are involved both in the aging process and in regulating lifespan. Here we outline a somatic cell depletion (SCD) model to account for correlations between: (1) mitochondrial reactive oxygen species and lifespan; (2) mitochondrial antioxidant enzymes and lifespan; (3) mitochondrial DNA mutation and lifespan and (4) cellular stress resistance and lifespan. We examine the available data from within the framework of the SCD model, in which mitochondrial dysfunction leading to cell death and gradual loss of essential somatic cells eventually contributes to the decline in physiological performance that limits lifespan. This model is useful in explaining many of the mitochondrial manipulations that alter maximum lifespan in a variety of animal species; however, there are a number of caveats and critical experiments outstanding, and these are outlined in this review.
Keywords: Mitochondria, lifespan, reactive oxygen species, superoxide dismutase, glutathione peroxidase, mtDNA, base excision repair, mutation
Current Aging Science
Title: Mitochondria, Cellular Stress Resistance, Somatic Cell Depletion and Lifespan
Volume: 2 Issue: 1
Author(s): Ellen L. Robb, Melissa M. Page and Jeffrey A. Stuart
Affiliation:
Keywords: Mitochondria, lifespan, reactive oxygen species, superoxide dismutase, glutathione peroxidase, mtDNA, base excision repair, mutation
Abstract: The causes of aging and determinants of maximum lifespan in animal species are multifaceted and complex. However, a wealth of experimental data suggests that mitochondria are involved both in the aging process and in regulating lifespan. Here we outline a somatic cell depletion (SCD) model to account for correlations between: (1) mitochondrial reactive oxygen species and lifespan; (2) mitochondrial antioxidant enzymes and lifespan; (3) mitochondrial DNA mutation and lifespan and (4) cellular stress resistance and lifespan. We examine the available data from within the framework of the SCD model, in which mitochondrial dysfunction leading to cell death and gradual loss of essential somatic cells eventually contributes to the decline in physiological performance that limits lifespan. This model is useful in explaining many of the mitochondrial manipulations that alter maximum lifespan in a variety of animal species; however, there are a number of caveats and critical experiments outstanding, and these are outlined in this review.
Export Options
About this article
Cite this article as:
Robb L. Ellen, Page M. Melissa and Stuart A. Jeffrey, Mitochondria, Cellular Stress Resistance, Somatic Cell Depletion and Lifespan, Current Aging Science 2009; 2 (1) . https://dx.doi.org/10.2174/1874609810902010012
DOI https://dx.doi.org/10.2174/1874609810902010012 |
Print ISSN 1874-6098 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-6128 |
- 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
-
Pharmacologic Therapy in Growth Hormone Disorders and the Heart
Current Medicinal Chemistry Caring for HIV-Infected Patients in the ICU in The Highly Active Antiretroviral Therapy Era
Current HIV Research Hypertension and Endothelial Dysfunction: Therapeutic Approach
Current Vascular Pharmacology Cardiomyocyte-Specific TβR2 Knockout Mice are More Susceptible to Cardiac Hypertrophy Induced by Adrenergic Agonist Stimulation
Current Molecular Medicine Targeting the Endocannabinod System to Limit Myocardial and Cerebral Ischemic and Reperfusion Injury
Current Pharmaceutical Biotechnology Malignancy and Radiation-Induced Cardiotoxicity
Cardiovascular & Hematological Disorders-Drug Targets Relationship of High-Sensitivity C-Reactive Protein Concentrations and Systolic Heart Failure
Current Vascular Pharmacology Interatrial Block in the Modern Era
Current Cardiology Reviews Cardiac Calmodulin Kinase: A Potential Target for Drug Design
Current Medicinal Chemistry NGS Technologies as a Turning Point in Rare Disease Research , Diagnosis and Treatment
Current Medicinal Chemistry CCR5 as a Potential Target in Cancer Therapy: Inhibition or Stimulation?
Anti-Cancer Agents in Medicinal Chemistry Contraception in Women with Medical Conditions
Current Women`s Health Reviews Prophylaxis of Cancer
Current Cancer Therapy Reviews Genetic Variations of the Hemostatic System as Risk Factors for Venous and Arterial Thrombotic Disease
Current Genomics Hypertension in Hemodialysis Patients
Current Hypertension Reviews Polymorphism Gln27Glu of β2 Adrenergic Receptors in Patients with Ischaemic Cardiomyopathy
Current Vascular Pharmacology Acute Kidney Injury in Pediatric Heart Failure
Current Cardiology Reviews Selectivity Problems with Drugs Acting on Cardiac Na<sup>+</sup> and Ca<sup>2+</sup> Channels
Current Medicinal Chemistry Interferon Treatment in Patients with Hypereosinophilia
Current Drug Targets Matrix Metalloproteinases as Valid Clinical Target
Current Pharmaceutical Design