Format

Send to

Choose Destination
Ageing Res Rev. 2019 Sep;54:100940. doi: 10.1016/j.arr.2019.100940. Epub 2019 Aug 12.

Mitochondria in the signaling pathways that control longevity and health span.

Author information

1
Center for Healthy Aging, Department of Cellular and Molecular Medicine, SUND, University of Copenhagen, 2200, Copenhagen N, Denmark.
2
Center for Healthy Aging, Department of Cellular and Molecular Medicine, SUND, University of Copenhagen, 2200, Copenhagen N, Denmark; Institute of Cell and Molecular Biosciences and Institute for Ageing, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK.
3
Center for Healthy Aging, Department of Cellular and Molecular Medicine, SUND, University of Copenhagen, 2200, Copenhagen N, Denmark; Laboratory of Molecular Gerontology, National Institute on Aging, 251 Bayview Blvd, Baltimore, USA. Electronic address: vbohr@nih.gov.

Abstract

Genetic and pharmacological intervention studies have identified evolutionarily conserved and functionally interconnected networks of cellular energy homeostasis, nutrient-sensing, and genome damage response signaling pathways, as prominent regulators of longevity and health span in various species. Mitochondria are the primary sites of ATP production and are key players in several other important cellular processes. Mitochondrial dysfunction diminishes tissue and organ functional performance and is a commonly considered feature of the aging process. Here we review the evidence that through reciprocal and multilevel functional interactions, mitochondria are implicated in the lifespan modulation function of these pathways, which altogether constitute a highly dynamic and complex system that controls the aging process. An important characteristic of these pathways is their extensive crosstalk and apparent malleability to modification by non-invasive pharmacological, dietary, and lifestyle interventions, with promising effects on lifespan and health span in animal models and potentially also in humans.

KEYWORDS:

Aging; DNA repair; Energy; Lifespan; Metabolism; Mitochondria

PMID:
31415807
DOI:
10.1016/j.arr.2019.100940

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center