Mitochondrial dysfunction is central in biological aging, but experimentally controlling mitochondria in vivo to test causality has been difficult. Optogenetically preserving mitochondrial function with age addressed this difficulty and increased lifespan and healthspan in Caenorhabditis elegans.
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Harman, D. The biologic clock: the mitochondria? J. Am. Geriatr. Soc. 20, 145–147 (1972). An early article proposing mitochondria as central in controlling the rate of aging.
Hughes, A. L. & Gottschling, D. E. An early age increase in vacuolar pH limits mitochondrial function and lifespan in yeast. Nature 492, 261–265 (2012). This paper reports an early decline in the mitochondrial proton gradient as causative for aging in the yeast model.
Berry, B. J. et al. Optogenetic control of mitochondrial protonmotive force to impact cellular stress resistance. EMBO Rep. 21, e49113 (2020). This paper was the first characterization of the light-powered mitochondria in C. elegans.
Zhang, H. et al. Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte. eLife 9, e60827 (2020). This paper implicates decreased mitochondrial proton gradient in mammalian tissue aging.
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This is a summary of: Berry, B. J. et al. Optogenetic rejuvenation of mitochondrial membrane potential extends C. elegans lifespan. Nat. Aging, https://doi.org/10.1038/s43587-022-00340-7 (2023).
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Harnessing light energy to charge mitochondria and extend lifespan. Nat Aging 3, 151–152 (2023). https://doi.org/10.1038/s43587-023-00364-7