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通过P2X7R/AKT/mTOR信号传导,高葡萄糖诱导的细胞自的降低.

Cheng Qian1, Jiayue Lu1, Xiajing Che1

  • 1Department of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Uremia Diagnosis and Treatment Center, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, PR China.

Free radical biology & medicine
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PubMed
概括
此摘要是机器生成的。

糖尿病病涉及细胞中纯能P2X7受体 (P2X7R) 的增加. 通过Akt-mTOR通路,P2X7R抑制了自,恶化了损伤. 向P2X7R可能治疗糖尿病病.

关键词:
这就是Akt信号.自自是一种自的过程.糖尿病 病 糖尿病 病这是一个P2X7RR.细胞是一种细胞.在mTOR信号传输中.

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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
  • 糖尿病学 糖尿病学

背景情况:

  • 糖尿病病是全球末期病的主要原因之一.
  • 在糖尿病患者中观察到尿中腺三酸盐 (ATP) 的增加.
  • purinergic受体在脏病理生理学中发挥作用.

研究的目的:

  • 研究纯能受体,特别是P2X7R在糖尿病病中的作用.
  • 阐明 P2X7R 影响葡萄细胞自和糖尿病损伤的机制.
  • 探索P2X7R作为糖尿病病的潜在治疗标.

主要方法:

  • 在野生型和P2X7R淘汰赛糖尿病小鼠的皮质中检查了纯能受体表达.
  • 评估了podocyte标记物 (podocin) 和自标记物 (LC-3II) 的表达.
  • 在高葡萄糖,P2X7RsiRNA和途径抑制剂 (Akt,mTOR) 暴露的体外 podocyte 培养物中使用.

主要成果:

  • 在糖尿病小鼠的皮质中,P2X7R的表达显著增加,并与 podocytes 共定位.
  • 在糖尿病脏中,P2X7R缺乏保留了多多的表达和正常化的LC-3II水平.
  • 通过Akt-mTOR激活,高葡萄糖降低了细胞自 (LC-3II降低,p62增加);P2X7R抑制/击退恢复了自.

结论:

  • 糖尿病细胞中的P2X7R增加有助于通过Akt-mTOR通路抑制自.
  • 这种P2X7R介导的自抑制会加剧细胞损伤,促进糖尿病病.
  • 准P2X7R是一种有前途的治疗策略,用于治疗糖尿病病.