Age-related declines in mitochondrial Prdx6 contribute to dysregulated muscle bioenergetics.

Jose Adan Arevalo, Dianna Xing, Roberto Garcia Leija, Max A Thorwald, Diana Daniela Moreno-Santillán, Kaitlin N Allen, Giovanna Selleghin-Veiga, Heidi C Avalos, Eva Utke, Justin L Conner, George A Brooks, José Pablo Vázquez-Medina

Department of Integrative Biology, University of California, Berkeley, USA.Department of Integrative Biology, University of California, Berkeley, USA. · pubmed

Paper

Abstract

An age-related decline in mitochondrial function is a multi-factorial hallmark of aging, driven partly by increased lipid hydroperoxide levels that impair mitochondrial respiration in skeletal muscle, leading to atrophy. Although pharmacological and genetic manipulations to counteract increased lipid hydroperoxide levels represent a promising strategy to treat sarcopenia, the mechanisms driving such phenotypes remain understudied. Peroxiredoxin 6 (Prdx6) is a multifunctional enzyme that contributes to peroxidized membrane repair via its phospholipid hydroperoxidase and phospholipase A

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Research summary

The paper claims that age-related declines in mitochondrial Prdx6 contribute to dysregulated muscle bioenergetics. This research addresses a potential root cause of aging-related muscle atrophy, which is relevant to understanding and potentially mitigating age-related decline in muscle function.

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