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在小鼠模型中糖尿病病中的细胞损伤涉及TRPC6介导的Calpain激活,损害了自
Yann Salemkour1, Dilemin Yildiz2, Léa Dionet1
1Université Paris Cité, Inserm, PARCC, Paris, France.
Journal of the American Society of Nephrology : JASN
|September 7, 2023
概括
糖尿病病通过TRPC6-介导的calpain激活损害了podocyte自. 用calpain抑制剂恢复自可以保护糖尿病小鼠免受损伤和蛋白尿.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 糖尿病病 (DKD) 的特点是受损的细胞自,这是细胞保护的关键过程.
- 独立于mTOR和AMPK通路的podocyte自的独特调节,使其在DKD中的机制不清楚.
研究的目的:
- 阐明通道TRPC6和囊蛋白酶calpains在DKD中podocyte自功能障碍中的作用.
- 研究TRPC6和calpain作为DKD的潜在治疗点.
主要方法:
- 研究了TRPC6和calpains对DKD小鼠模型中的Podocyte自的影响.
- 在体内研究中使用了链毒素诱导和BTBR异位/异位小鼠模型.
- 评估了自流,细胞损伤标志物 (尼弗林) 和白色素尿.
主要成果:
- 在小鼠中,糖尿病增加了TRPC6表达和受损的podocyte自流.
- 通过减少calpain活动,TRPC6敲击增强了自流.
- 抑制calpain或过度表达calpastatin正常化了自,减少了nephrin损失,并防止了albuminuria.
- 人类脏活检显示TRPC6,降低卡尔巴斯塔丁,自阻塞和podocyte损伤之间的相关性.
结论:
- 确定了一种新机制,将TRPC6和calpain活性与DKD中受损的Podocyte自性联系起来.
- 通过向TRPC6和/或calpains恢复podocyte自,为DKD提供了一个有前途的治疗策略.
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