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Caveolae are intracellular vesicles with diameters ranging from 50 to 100 nm. The role of caveolins in mediating oxidative stress, autophagy, apoptosis, fibrosis, and vascular remodeling has attracted increasing attention in cardiovascular therapy. Several studies have suggested that caveolin could be a therapeutic target for the treatment of cardiac and/or vascular injury via several pathophysiological mechanisms. Despite substantial advances in our understanding of the basic biology of vesicles over the past decade, the relevance and specific role of these mechanisms in cardiovascular homeostasis remains ambiguous. Here, we review the macroscopic role of caveolins in protecting cardiac function and, at the microscopic level, examine possible cardioprotective caveolar mechanisms, including their antioxidative stress, antiapoptosis, autophagy-regulatory, antifibrosis, and angiogenesis-promoting properties. We believe that the role of caveolins in cardiac functioning has not been fully elucidated and is an important line of future research with several cardioprotective implications.
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http://dx.doi.org/10.1111/febs.16798 | DOI Listing |
J Biol Chem
August 2025
DAMP Laboratory, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 510150, China. Electronic address:
Ciprofloxacin (CFX) is a broad-spectrum antibiotic belonging to the fluoroquinolone class, widely used to treat bacterial infections by inhibiting bacterial DNA replication. Ferroptosis, a form of regulated cell death, is characterized by lipid peroxidation on cellular and organelle membranes. Our previous studies demonstrated that ciprofloxacin inhibits erastin-induced ferroptosis by enhancing glutathione peroxidase 4 (GPX4) protein stability.
View Article and Find Full Text PDFJ Infect Dis
September 2025
Indian Institute of Science Education and Research (IISER) Bhopal, Bhopal, MP, India.
Chandipura virus (CHPV), a Rhabdoviridae family member, is an emerging neurotropic pathogen responsible for acute encephalitis outbreaks in children, mainly in India. Despite its public health relevance, the mechanisms underlying CHPV entry into host cells remain poorly understood. In this study, we used pharmacological inhibitors in Vero cells to dissect the virus's entry pathways.
View Article and Find Full Text PDFCell Death Dis
August 2025
Department of Gastroenterology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Caveolin-1 (CAV1), a pivotal protein implicated in endothelial cell-mediated angiogenesis, assumes an ambiguous role with elusive underlying mechanisms in the pathogenesis of inflammatory bowel disease (IBD). In this investigation, we delineated the involvement of CAV1 in murine models of dextran sulfate sodium (DSS)-induced colitis. CAV1 knockout mice manifested attenuated pathological and inflammatory damage to the epithelium, whereas mice overexpressing CAV1 exhibited contrasting outcomes.
View Article and Find Full Text PDFMedicine (Baltimore)
August 2025
Department of Biochemistry and Molecular Biology, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi, Xinjiang, China.
Long noncoding RNAs (LncRNAs) play critical roles in regulating gene expression and cellular processes, including adipocyte differentiation. LncRNA00602 is upregulated in adipose tissue. Therefore, we aimed to investigate the potential role of LncRNA00602 in adenovirus type 36 (Ad36)-induced adipocyte browning.
View Article and Find Full Text PDFJ Infect Dis
August 2025
Department of Biological Sciences, Centre for Cell Biology, Development, and Disease (C2D2), 8888 University Drive, Simon Fraser University, Burnaby, BC, Canada.
Listeria monocytogenes spreads intercellularly by creating actin-rich projections that are endocytosed into recipient cells. Caveolin-mediated endocytosis has been implicated in this process, accounting for ∼70% in cell-to-cell spread in cells depleted of caveolin-1. Thus, additional mechanisms may contribute for the remaining spread and we examined the role of flotillin-based endocytosis.
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