Mild mitochondrial impairment enhances innate immunity and longevity through ATFS-1 and p38 signaling.

ABSTRACT: While mitochondrial function is essential for life in all multicellular organisms, a mild impairment of mitochondrial function can extend longevity in model organisms. By understanding the molecular mechanisms involved, these pathways might be targeted to promote healthy aging. In studying two long-lived mitochondrial mutants in C. elegans, we found that disrupting subunits of the mitochondrial electron transport chain results in upregulation of genes involved in innate immunity, which is driven by the mitochondrial unfolded protein response (mitoUPR) but also dependent on the canonical p38-mediated innate immune signaling pathway. Both of these pathways are required for the increased resistance to bacterial pathogens and extended longevity of the long-lived mitochondrial mutants, as is th

SUBMITTER: Campos JC 

PROVIDER: S-EPMC8647147 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature