ArticleNature communications2026
Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Article
- Neuronal expression of bromodomain proteins alters neuronal health and peripheral protein homeostasis to promote longevity.Genes & development · 2026Article
- Effects of Red Onion Peel Extracts on Oxidative Stress inBiomolecules · 2026Article
- Mitochondrial Dysfunction in Circulating Blood Cells and Biological Aging: A Review of Mechanisms and Evidence.Biomolecules · 2026Review
- New molecular players: siRNA expression and gene regulation in Hordeum vulgare L. ageing seeds after germination.BMC genomics · 2026Article
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13 authors.
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Abstract
Mitochondrial dysfunction is a prominent hallmark of aging contributing to the decline of metabolic plasticity in late life. While genetic distortions of mitochondrial integrity elicit premature aging, the mechanisms leading to "natural" aging of mitochondria are less clear. Here we use proteomics, lipidomics, genetics and functional tests in wild type Caenorhabditis elegans and long-lived clk-1(qm30) and isp-1(qm150) mitochondrial mutants to identify molecular pathways that support longevity amid persistent mitochondrial inefficiency. These tests and subsequent transcriptomics and metabolomics analyses in humans reveal aging-associated decline of phosphatidylcholine synthesis as a trigger of mitochondrial network disruption, which contributes to mitochondrial dysfunction during normal aging. Moreover, ectopic boosting of phosphatidylcholine levels via diet restores late life mitochondrial integrity in vivo in nematodes and reinstates metabolic resilience in human cell culture tests. We thus describe a previously unrecognized natural driver of mitochondrial decline in aging that is malleable by dietary interventions.
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