Recent studies have assessed the role of angiotensin II in apoptosis and the effects of the angiotensin II type 1 (AT1) and type 2 (AT2) receptor subtypes. A complex picture is emerging with cell-specific effects of AT1 and AT2 receptors, and differential effects dependent on pathology. In vitro studies have shown that angiotensin II mediated apoptosis in myocytes and endothelium. More recent in vivo studies have shown the prevention and regression of vascular lesions by apoptosis induction with medications (including AT1 receptor inhibitor).
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BMC Biol
January 2025
Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Background: Extracellular vesicles (EVs) derived from endothelial cells (ECs) are increasingly recognized for their role in the initiation and progression of atherosclerosis. ECs experience varying degrees and types of blood flow depending on their specific arterial locations. In regions of disturbed flow, which are predominant sites for atherosclerotic plaque formation, the impact of disturbed flow on the secretion and function of ECs-derived EVs remains unclear.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Pediatrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), NHC Key Laboratory of Chronobiology, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Recent advancements in the mechanistic comprehension of vascular biology have concentrated on METTL3-mediated N-methyladenosine modification of RNA, which modulates a spectrum of RNA functionalities with precision. Despite extensive investigations into the roles and mechanisms of METTL3 within vascular biology, a holistic review elucidating their interconnections remains absent. This analysis endeavors to meticulously scrutinize the involvement of METTL3 in both the physiological and pathological paradigms of vascular biology.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
Department of Aerospace Medical Training, School of Aerospace Medicine, Fourth Military Medical University, 169 Chang Le Xi Road, Xi'an, 710032, China.
Background: Prolonged spaceflight is known to cause vascular deconditioning and remodeling. Tail suspension, a widely used spaceflight analog, is reported to result in vascular remodeling of rats. However, little is known about the cellular atlas of the heterogeneous cells of CA and FA from hindlimb-unloaded rats.
View Article and Find Full Text PDFActa Pharmacol Sin
January 2025
Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, China.
Increased level of angiotensin II (Ang II) plays a central role in the development of hypertensive vascular remodeling. In this study, we identified the deubiquitinating enzyme Josephin domain-containing protein 2 (JOSD2) as a protective factor and investigated its molecular mechanism in Ang II-induced vascular remodeling. First, we found that JOSD2 was upregulated in aortic smooth muscle cells, but not in endothelial cells of Ang II-challenged mouse vascular tissues.
View Article and Find Full Text PDFPharmacol Rep
January 2025
Center for Global Health Research, Saveetha Medical College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai, India.
Cardiovascular illnesses are multifactorial disorders and represent the primary reasons for death worldwide, according to the World Health Organization. As a signaling molecule, nitric oxide (NO) is extremely permeable across cellular membranes owing to its unique molecular features, like its small molecular size, lipophilicity, and free radical properties. Some of the biological effects of NO are vasodilation, inhibition in the growth of vascular smooth muscle cells, and functional regulation of cardiac cells.
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