🧬 SinoBioData Academic Portal
Official PDF TranslationActa Biochimica et Biophysica Sinica

P300-mediated H3K18 acetylation triggers necroptosis via modulation of KRT18 transcription in diabetic nephropathy

Authors: Qiao Zhao; Qinqin Cai; Aynigar Nizam; Qingxia Yang; Xu Liu; Fufen Meng; Zhipeng Meng

DOI: 10.3724/abbs.2026015Status: Verified Translated Edition
Sponsored AdvertisementAd Placement Area
reCAPTCHA Bot Shield Active

Preparing Secure Academic Download

Verifying human reader & generating high-resolution document...

Verifying Document Integrity15s remaining
← Back to Article
Protected by Google reCAPTCHA v3.PrivacyTerms
Sponsored ContentAdSense In-Feed Ad Slot

Key Findings in This Report

• P300 and H3K18ac are upregulated in diabetic nephropathy, correlating with increased KRT18 expression and necroptosis. • P300 directly regulates KRT18 transcription via H3K18 acetylation, driving RIPK1/MLKL-mediated necroptosis in tubular epithelial cells. • Inhibition of P300 with C646 or knockdown of P300/KRT18 attenuates necroptosis and may represent a therapeutic strategy for DN. • The P300-KRT18 axis is a novel epigenetic mechanism contributing to DN progression, offering potential targets for intervention.
Download Full PDF: P300-mediated H3K18 acetylation triggers necroptosis via modulation of KRT18 transcription in diabetic nephropathy | SinoBioData | SinoBioData