Khovantseva Ulyana, Kiseleva Diana, Cherednichenko Vadim, Chakal Deyyara, Breshenkov Denis, Markina Yuliya, Ziganshin Rustam, Charchyan Eduard, Markin Alexander
Petrovsky National Research Center of Surgery, 119435, Moscow, Russian Federation.
Lomonosov Moscow State University, 119991, Moscow, Russian Federation.
Sci Rep. 2025 Jul 22;15(1):26596. doi: 10.1038/s41598-025-11345-8.
Cardiovascular diseases (CVD) are one of the leading causes of death worldwide. From a modern point of view, endothelial dysfunction is considered as a key factor leading to the development of CVD. However, scientists have suggested that the main causes of the development of CVD might be functional disorders and phenotypic modulation of smooth muscle cells (SMCs) that make up the vascular wall. In this regard, the aim of our study was to evaluate the functional features of SMCs isolated from the tunica intima and from the tunica media of the thoracic part of the human aorta in patients with CVD. In our research we showed that phenotypic switching can occur in SMCs isolated from patients with aneurysms (n = 6), resulting in remodeling of the extracellular matrix and impaired interaction between cellular receptors. In addition, it is probable that the activation of complement-mediated phagocytosis as a result of LDL internalization by SMCs might be one of the key mechanisms in the process of aneurysm development.
心血管疾病(CVD)是全球主要死因之一。从现代观点来看,内皮功能障碍被认为是导致心血管疾病发展的关键因素。然而,科学家们提出,心血管疾病发展的主要原因可能是构成血管壁的平滑肌细胞(SMC)的功能紊乱和表型调节。在这方面,我们研究的目的是评估从患有心血管疾病患者的人主动脉胸段内膜和中膜分离出的平滑肌细胞的功能特征。在我们的研究中,我们发现从动脉瘤患者(n = 6)分离出的平滑肌细胞中可能发生表型转换,导致细胞外基质重塑以及细胞受体之间的相互作用受损。此外,平滑肌细胞内化低密度脂蛋白(LDL)导致补体介导的吞噬作用激活,这可能是动脉瘤发展过程中的关键机制之一。