Hypertensive Nephropathy: Unveiling the Possible Involvement of Hemichannels and Pannexons
Journal
International Journal of Molecular Sciences
ISSN
1422-0067
Date Issued
2022
Author(s)
Claudia M. Lucero
Juan Prieto-Villalobos
Lucas Marambio-Ruiz
Javiera Balmazabal
Tanhia F. Alvear
Matías Vega
Paola Barra
Juan A. Orellana
Gonzalo I. Gómez
Type
Resource Types::text::journal::journal article
URL Institutional Repository
Abstract
<jats:p>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.</jats:p>
Cite this document
Lucero, C. M., Prieto-Villalobos, J., Marambio-Ruiz, L., Balmazabal, J., Alvear, T. F., Vega, M., Barra, P., Retamal, M. A., Orellana, J. A., & Gómez, G. I. (2022). Hypertensive nephropathy: Unveiling the possible involvement of hemichannels and pannexons. International Journal of Molecular Sciences, 23(24), 15936. https://doi.org/10.3390/ijms232415936
Subjects
ca<sup>2+</sup> dynamics
;
connexin 43 hemichannel
;
gap junctions
;
hypertensive nephropathy
;
inflammation
;
oxidative stress
;
pannexins 1 channels
;
angiotensin ii
;
animals
;
connexins
;
gap junctions
;
humans
;
hypertension, renal
;
nephritis
;
adenosine triphosphate
;
aldosterone
;
angiotensin 1a receptor
;
angiotensin ii
;
angiotensin receptor
;
calcium ion
;
cell adhesion molecule
;
chemokine
;
collagen
;
collagen type 4
;
connexin 43
;
cytokine
;
dipeptidyl carboxypeptidase
;
fibronectin
;
gap junction protein
;
glucose
;
interleukin 1beta
;
laminin
;
monocyte chemotactic protein 1
;
osteopontin
;
pannexin
;
purinergic receptor
;
reactive oxygen metabolite
;
reduced nicotinamide adenine dinucleotide phosphate oxidase
;
renin
;
scleroprotein
;
transforming growth factor beta1
;
tumor necrosis factor
;
unclassified drug
;
angiotensin ii
;
gap junction protein
;
acute kidney failure
;
blood pressure
;
blood vessel tone
;
calcium homeostasis
;
cardiovascular disease
;
cell damage
;
chronic kidney failure
;
connexon
;
deregulation
;
diabetes mellitus
;
disease course
;
end stage renal disease
;
experimental model
;
fibroblast
;
gap junction
;
glomerular filtration barrier
;
glomerulonephritis
;
glomerulosclerosis
;
glomerulus filtration rate
;
human
;
hypertension
;
hypertensive nephropathy
;
inflammation
;
invertebrate
;
kidney blood flow
;
kidney fibrosis
;
kidney injury
;
kidney polycystic disease
;
kidney tubule necrosis
;
mechanical stress
;
mesangium cell
;
nonhuman
;
oxidative stress
;
pathogenesis
;
proliferative glomerulonephritis
;
renin angiotensin aldosterone system
;
review
;
risk factor
;
second messenger
;
signal transduction
;
ureter obstruction
;
vertebrate
;
animal
;
gap junction
;
nephritis
;
physiology
;
renovascular hypertension