|Age-related decline in mitochondrial bioenergetics: does supercomplex destabilization determine lower oxidative capacity and higher superoxide production?
|Year of Publication
|Gómez LA, Hagen TM
|Semin Cell Dev Biol
|Aging, Animals, Energy Metabolism, Humans, Lipid Metabolism, Mitochondria, Oxidative Stress, Superoxides
Mitochondrial decay plays a central role in the aging process. Although certainly multifactorial in nature, defective operation of the electron transport chain (ETC) constitutes a key mechanism involved in the age-associated loss of mitochondrial energy metabolism. Primarily, mitochondrial dysfunction affects the aging animal by limiting bioenergetic reserve capacity and/or increasing oxidative stress via enhanced electron leakage from the ETC. Even though the important aging characteristics of mitochondrial decay are known, the molecular events underlying inefficient electron flux that ultimately leads to higher superoxide appearance and impaired respiration are not completely understood. This review focuses on the potential role(s) that age-associated destabilization of the macromolecular organization of the ETC (i.e. supercomplexes) may be important for development of the mitochondrial aging phenotype, particularly in post-mitotic tissues.
|Semin. Cell Dev. Biol.
|PubMed Central ID
|R01 AG017141 / AG / NIA NIH HHS / United States
P01AT002034 / AT / NCCIH NIH HHS / United States
2R01AG017141-06A2 / AG / NIA NIH HHS / United States
ES00240 / ES / NIEHS NIH HHS / United States
P01 AT002034 / AT / NCCIH NIH HHS / United States