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Deacetylation of Septin4 by SIRT2 (Silent Mating Type Information Regulation 2 Homolog-2) Mitigates Damaging of Hypertensive Nephropathy.

Ying ZhangNaijin ZhangYuanming ZouChunyu SongKexin CaoBoquan WuShilong YouSaien LuDong WangJiaqi XuXinyue HuangPengyu ZhangZihao FanJingwei LiuZhongyi ChengZhe ZhangChuize KongLiu CaoYing-Xian Sun
Published in: Circulation research (2023)
Septin4, when activated through acetylation of K174 (K174Q), promotes hypertensive renal injury. Septin4-K174R, which mimics deacetylation by SIRT2, inhibits the cleaved-PARP1-cleaved-caspase3 pathway. Septin4-K174R acts as a renal protective factor, mitigating Ang II-induced hypertensive renal injury. These findings indicate that septin4-K174 is a potential therapeutic target for the treatment of hypertensive renal injury.
Keyphrases
  • blood pressure
  • oxidative stress
  • cell death
  • dna damage
  • ischemia reperfusion injury
  • healthcare
  • angiotensin ii
  • risk assessment
  • diabetic rats
  • induced apoptosis
  • social media
  • endoplasmic reticulum stress
  • stress induced