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Integrin subunit alpha 5 maintains mitochondrial function in ox-LDL-induced cardiac microvascular endothelial cells via activating the PI3K/AKT signaling pathway.
Wang, Xianfeng; Mao, Wenkai; Ma, Xiaofeng.
Afiliación
  • Wang X; Emergency Department, Qinghai Cardio-Cerebrovascular Specialty Hospital, Qinghai High Altitude Medical Research Institute, Xining, Qinghai 810012, P.R. China.
  • Mao W; Medical Department, Qinghai Cardio-Cerebrovascular Specialty Hospital, Qinghai High Altitude Medical Research Institute, Xining, Qinghai 810012, P.R. China.
  • Ma X; Personnel Department, Qinghai Cardio-Cerebrovascular Specialty Hospital, Qinghai High Altitude Medical Research Institute, Xining, Qinghai 810012, P.R. China. Maxiaofeng921113@163.com.
Folia Morphol (Warsz) ; 2024 May 17.
Article en En | MEDLINE | ID: mdl-38757500
ABSTRACT
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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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Folia Morphol (Warsz) Año: 2024 Tipo del documento: Article Pais de publicación: Polonia
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Folia Morphol (Warsz) Año: 2024 Tipo del documento: Article Pais de publicación: Polonia