Abstract
Hypertension is one of the most common risk factors for developing chronic cardiovascular diseases, including hypertensive nephropathy. Within the glomerulus, hypertension causes damage and activation of mesangial cells (MCs), eliciting the production of large amounts of vasoactive and proinflammatory agents. Accordingly, the activation of AT1 receptors by the vasoactive molecule angiotensin II (AngII) contributes to the pathogenesis of renal damage, which is mediated mostly by the dysfunction of intracellular Ca2+ ([Ca2+]i) signaling. Similarly, inflammation entails complex processes, where [Ca2+]i also play crucial roles. Deregulation of this second messenger increases cell damage and promotes fibrosis, reduces renal blood flow, and impairs the glomerular filtration barrier. In vertebrates, [Ca2+]i signaling depends, in part, on the activity of two families of large-pore channels: hemichannels and pannexons. Interestingly, the opening of these channels depends on [Ca2+]i signaling. In this review, we propose that the opening of channels formed by connexins and/or pannexins mediated by AngII induces the ATP release to the extracellular media, with the subsequent activation of purinergic receptors. This process could elicit Ca2+ overload and constitute a feed-forward mechanism, leading to kidney damage.
Subject
Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis
Reference165 articles.
1. Renal physiology;Atherton;Br. J. Anaesth.,1972
2. Circadian Rhythms and Renal Pathophysiology;Mohandas;J. Clin. Investig.,2022
3. New Insights into the Dynamic Regulation of Water and Acid-Base Balance by Renal Epithelial Cells.o Title;Brown;Am. J. Physiol. Cell Physiol.,2012
4. Lv, J.-C., and Zhang, L.-X. (2019). Renal Fibrosis: Mechanisms and Therapies, Springer.
5. The Kidney, a Cardiovascular Risk Marker, and a New Target for Therapy;Hillege;Kidney Int. Suppl.,2005
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献