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阿佩林/APJ通过通过SIRT3‐KLF15改善质内皮细胞功能障碍来缓解糖尿病病

Mingcong Huang¹, Jing Chang², Yu Liu³

¹Department of Physiology and Pathophysiology, Capital Medical University, Beijing 100069, P.R. China.

Molecular medicine reports

|March 7, 2025

概括

阿佩林/APJ信号通过抑制细胞中的细胞外基质合成来减少糖尿病病中球底膜的厚化. 这一途径涉及SIRT3和KLF15,为糖尿病病提供了潜在的治疗标.

科学领域:

腎臟病學 (nephrology) 是一種醫學.
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

糖尿病病 (DN) 的特征是质底膜 (GBM) 变厚,与质内皮细胞 (GEC) 功能障碍和细胞外基质 (ECM) 合成增加有关.
内源性的阿佩林及其受体 (APJ) 显示出缓解DN内皮细胞功能障碍的潜力.

研究的目的:

通过减少 GEC 中的 ECM 合成,研究该假设,即阿佩林/APJ 途径减少了 GBM 加厚.
阐明阿佩林/APJ在糖尿病病中的保护作用背后的分子机制.

主要方法:

利用糖尿病小鼠模型和GEC来评估阿佩林治疗和APJ淘汰赛的影响.
量化的GBM加厚和ECM成分的表达 (胺,原IV).
研究了SIRT3和KLF15在调解阿佩林/APJ信号传递中的作用.

主要成果:

在糖尿病小鼠中,阿佩林的使用可通过降低拉米因和原IV表达来降低球纤维化和GBM加厚.
这些影响在GEC中被废除了APJ淘汰赛.
阿佩林/APJ信号增强了SIRT3的表达和活性,促进了KLF15脱乙和核转位,从而抑制了拉米林和原IV合成.

结论:

阿佩林/APJ信号有效地减少了糖尿病病中的GBM加厚.
保护机制涉及通过GEC中的SIRT3-KLF15通路抑制拉敏和原IV合成.
针对阿佩林/APJ-SIRT3-KLF15轴为糖尿病病提供了一个有前途的治疗策略.

关键词:

这就是阿佩林 (apelin) 的意思.糖尿病性脏病糖尿病脏病内皮细胞是内皮细胞.细胞外矩阵是细胞外矩阵.球体底层膜的球体底层膜.

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