ArticleProceedings of the National Academy of Sciences of the United States of America2025
Rac1 promotes proximal tubule kidney repair by coupling the actin cytoskeleton to mitochondrial function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Sigma-1 receptor protects against renal ischemia-reperfusion injury by enhancing mitophagy via Rac1 regulation.Renal failure · 2026Article
- ELMO1 dependent efferocytosis protects from nephrotoxin induced acute kidney injury.Cell death discovery · 2026Article
- Rho/ROCK Signaling Pathway in Kidney Diseases: Mechanisms and Therapeutic Perspectives.Biomedicines · 2026Review
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Authors and funding
24 authors.
Funding
Abstract
The kidney proximal tubule (PT) is a specialized polarized epithelium that functions as a high capacity resorptive machine. PT cells are exquisitely sensitive to ischemia due to their high metabolic rate. The small GTPase Rac1 regulates epithelial function by promoting polarity through its effects on the actin cytoskeleton. We show that Rac1, in the setting of the recovery of the PT from ischemic injury, plays a critical role in reconstituting cellular bioenergetics by promoting actin cytoskeleton formation around damaged mitochondria. This mechanism removes damaged mitochondria through mitophagy and preserves PT metabolic capacity and reabsorption function. Loss of Rac1 causes intracellular lipid accumulation, energy depletion, and PT cell atrophy. Thus, Rac1 promotes the repair of PT cells by enhancing mitochondrial bioenergetics, rather than by regulating cell polarity via a mechanism that links the actin cytoskeleton to metabolic demands and cell morphology.
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