| Full text | |
| Author(s): |
Total Authors: 3
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| Affiliation: | [1] Univ Sao Paulo, Inst Quim, Dept Bioquim, Lab Genet Mitocondrial, Ave Prof Lineu Prestes, 748 Bloco 10S, Sala 1070, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Estadual Campinas, Fac Med, Dept Patol Clin, Campinas - Brazil
Total Affiliations: 2
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| Document type: | Journal article |
| Source: | Antioxidants & Redox Signaling; JAN 2022. |
| Web of Science Citations: | 0 |
| Abstract | |
Significance: Aging is a natural process that affects most living organisms, resulting in increased mortality. As the world population ages, the prevalence of age-associated diseases, and their associated health care costs, has increased sharply. A better understanding of the molecular mechanisms that lead to cellular dysfunction may provide important targets for interventions to prevent or treat these diseases.Recent Advances: Although the mitochondrial theory of aging had been proposed more than 40 years ago, recent new data have given stronger support for a central role for mitochondrial dysfunction in several pathways that are deregulated during normal aging and age-associated disease.Critical Issues: Several of the experimental evidence linking mitochondrial alterations to age-associated loss of function are correlative and mechanistic insights are still elusive. Here, we review how mitochondrial dysfunction may be involved in many of the known hallmarks of aging, and how these pathways interact in an intricate net of molecular relationships.Future Directions: As it has become clear that mitochondrial dysfunction plays causative roles in normal aging and age-associated diseases, it is necessary to better define the molecular interactions and the temporal and causal relationship between these changes and the relevant phenotypes seen during the aging process. (AU) | |
| FAPESP's process: | 17/04372-0 - Mitochondrial DNA: mechanisms for genome integrity maintenance and impact on disease |
| Grantee: | Nadja Cristhina de Souza Pinto |
| Support Opportunities: | Research Projects - Thematic Grants |
| FAPESP's process: | 17/17728-8 - Mitochondrial function and dysfunction: implications for aging and associated diseases |
| Grantee: | Aníbal Eugênio Vercesi |
| Support Opportunities: | Research Projects - Thematic Grants |