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Genetic and pharmaceutical targeting of Suv39h1 ameliorates renal fibrosis by unlocking CXCL10 transcription
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DOI：10.1016/j.jare.2026.08.032.png)
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Abstract
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• Suv39h1 is transcriptionally activated during fibroblast-myofibroblast transition. • Suv39h1 deletion in fibroblasts/myofibroblasts attenuates renal fibrosis in mice. • Suv39h1 inhibition by chaetocin alleviates renal fibrosis in mice. • Transcriptomic screening identifies CXCL10 as a novel target for Suv39h1. • CXCL10 suppresses FMyT by modulating the Hippo-YAP signaling.
Keywords:
Renal fibrosis
Fibroblast
Myofibroblast
Transcriptional regulation
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