整合素亚基α5通过激活PI3K/AKT信号通路维持氧化-LDL诱导的心脏微血管内皮细胞的线粒体功能。

IF 1.2 4区 医学 Q3 ANATOMY & MORPHOLOGY
Xianfeng Wang, Wenkai Mao, Xiaofeng Ma
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引用次数: 0

摘要

心脏微血管内皮细胞(CMECs)在血流调节中起着关键作用,其功能受损会引发一系列病理变化。我们之前的研究发现,通过整合素蛋白家族成员整合素亚基α5(ITGA5)的干预,可显著缓解 CMECs 的功能障碍。本研究探讨了 ITGA5 对 CMECs 线粒体功能的影响,并揭示了其调控途径。用氧化低密度脂蛋白(ox-LDL)刺激 CMEC,模拟冠状动脉疾病(CAD)。研究人员系统地确定了 ITGA5 对 CMEC 不同方面行为的影响,包括活力、凋亡、血管生成、氧化应激和线粒体功能。以磷脂酰肌醇 3- 激酶(PI3K)/Akt 信号通路为研究重点,利用 PI3K 抑制剂 LY294002 证实了该通路的中介作用。ITGA5 的过表达对氧化-LDL 诱导的 CMECs 损害有缓解作用,表现为活力、血管生成、线粒体功能增强,凋亡和氧化应激减少。PI3K 抑制剂对这些有益作用的反作用证明了 PI3K/AKT 信号通路的参与。总之,本研究发现,ITGA5 可激活 PI3k/Akt 信号通路,从而协调线粒体功能并减轻氧化-LDL 诱导的 CMEC 功能障碍。因此,有针对性地改善这种细胞损伤是预防和改善这种疾病的一项具有战略意义的关键工作。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Integrin subunit alpha 5 maintains mitochondrial function in ox-LDL-induced cardiac microvascular endothelial cells via activating the PI3K/AKT signaling pathway.

Cardiac microvascular endothelial cells (CMECs) assume a pivotal role in the regulation of blood flow, and their impairment precipitates a spectrum of pathological transformations. Our previous study unveiled a notable mitigation of CMECs dysfunction through the intervention of integrin subunit alpha 5 (ITGA5), a member of the integrin protein family. This study delves into the effect of ITGA5 on the mitochondrial function in CMECs and reveals the regulation pathway. CMECs were stimulated with oxidized low-density lipoprotein (ox-LDL) to mimic coronary artery disease (CAD). The effects of ITGA5 on diverse facets of CMEC behavior, encompassing viability, apoptosis, angiogenesis, oxidative stress, and mitochondrial function, was systematically ascertained. Employing the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway as a focal point of investigation, the mediation of this pathway was substantiated utilizing the PI3K inhibitor LY294002. ITGA5 overexpression exerted a mitigating influence upon the ox-LDL-induced detriment to CMECs, manifested as increased viability, angiogenesis, mitochondrial function, and diminished apoptosis and oxidative stress. The counteraction of these salubrious effects by the administration of the PI3K inhibitor attests to the engagement of the PI3K/AKT signaling pathway. Overall, this study has discerned that ITGA5 activates the PI3k/Akt signaling pathway to orchestrate mitochondrial function and diminish ox-LDL-induced CMEC dysfunction. Thus, the targeted amelioration of this cellular injury emerges as a strategically pivotal endeavor for the prevention and amelioration of this ailment.

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来源期刊
Folia morphologica
Folia morphologica ANATOMY & MORPHOLOGY-
CiteScore
2.40
自引率
0.00%
发文量
218
审稿时长
6-12 weeks
期刊介绍: "Folia Morphologica" is an official journal of the Polish Anatomical Society (a Constituent Member of European Federation for Experimental Morphology - EFEM). It contains original articles and reviews on morphology in the broadest sense (descriptive, experimental, and methodological). Papers dealing with practical application of morphological research to clinical problems may also be considered. Full-length papers as well as short research notes can be submitted. Descriptive papers dealing with non-mammals, cannot be accepted for publication with some exception.
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