Rho GTPases in kidney physiology and diseases.
Rho GTPases
cytoskeletal dynamics
diabetes
nephropathies
podocytes
Journal
Small GTPases
ISSN: 2154-1256
Titre abrégé: Small GTPases
Pays: United States
ID NLM: 101530974
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
pubmed:
18
6
2021
medline:
1
12
2022
entrez:
17
6
2021
Statut:
ppublish
Résumé
Rho family GTPases are molecular switches best known for their pivotal role in dynamic regulation of the actin cytoskeleton, but also of cellular morphology, motility, adhesion and proliferation. The prototypic members of this family (RhoA, Rac1 and Cdc42) also contribute to the normal kidney function and play important roles in the structure and function of various kidney cells including tubular epithelial cells, mesangial cells and podocytes. The kidney's vital filtration function depends on the structural integrity of the glomerulus, the proximal portion of the nephron. Within the glomerulus, the architecturally actin-based cytoskeleton podocyte forms the final cellular barrier to filtration. The glomerulus appears as a highly dynamic signalling hub that is capable of integrating intracellular cues from its individual structural components. Dynamic regulation of the podocyte cytoskeleton is required for efficient barrier function of the kidney. As master regulators of actin cytoskeletal dynamics, Rho GTPases are therefore of critical importance for sustained kidney barrier function. Dysregulated activities of the Rho GTPases and of their effectors are implicated in the pathogenesis of both hereditary and idiopathic forms of kidney diseases. Diabetic nephropathy is a progressive kidney disease that is caused by injury to kidney glomeruli. High glucose activates RhoA/Rho-kinase in mesangial cells, leading to excessive extracellular matrix production (glomerulosclerosis). This RhoA/Rho-kinase pathway also seems involved in the post-transplant hypertension frequently observed during treatment with calcineurin inhibitors, whereas Rac1 activation was observed in post-transplant ischaemic acute kidney injury.
Identifiants
pubmed: 34138686
doi: 10.1080/21541248.2021.1932402
pmc: PMC9707548
doi:
Substances chimiques
rho GTP-Binding Proteins
EC 3.6.5.2
Actins
0
rho-Associated Kinases
EC 2.7.11.1
rac1 GTP-Binding Protein
EC 3.6.5.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
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