ArticleNature communications2025
Methionine restriction alleviates kidney fibrosis through epigenetic repression of the TGF-β-Smad3-Hoxc8/P-TEFb axis.
Article in Nature communications, 2025. 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.
- Amino acid homeostasis in the kidney: Physiological roles and pathological dysregulation.Physiological reports · 2026Review
- Protective Effects of Lactobacillus Reuteri Isolated from Goats in a Murine Model of Salmonella Infection.Probiotics and antimicrobial proteins · 2026Article
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Nutritional methionine restriction modulates gut microbiota and propionate/GPR41 signaling to mitigate diabetic kidney disease.NPJ science of food · 2026Article
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Low-protein diets can mitigate renal fibrosis, yet the critical amino acids responsible for this benefit and its underlying mechanism remain unclear. Using exclusively male mice throughout this study, we screen 15 amino acid-restricted diets in a unilateral ureteral obstruction model and identify methionine restriction (MetR) as the most effective intervention. Integrating transcriptomic and cistromic analyses identify Hoxc8 as a central pro-fibrotic transcription factor downstream of TGF-β-Smad3 signaling. Hoxc8 reinforces its own expression and drives fibrotic gene programs through recruitment of the P-TEFb transcriptional elongation complex. HOXC8 is elevated in fibrotic human kidneys, and fibroblast-specific Hoxc8 deletion protects mice from renal fibrosis. MetR suppresses this pro-fibrotic circuit by reducing active histone marks at the Hoxc8 locus, thereby attenuating Hoxc8-dependent transcription. Together, these findings identify the TGF-β-Smad3-Hoxc8/P-TEFb axis as a key driver of renal fibrosis and highlight MetR as a promising therapeutic strategy.
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Registered trials
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