Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9339
Title: Apoptosis and angiotensin II: yet another renal regulatory system?
Austin Authors: Bonnet, Fabrice;Cao, Zemin;Cooper, Mark E
Affiliation: Department of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg West, Victoria, Australia
Issue Date: 2001
Publication information: Experimental Nephrology; 9(5): 295-300
Abstract: Apoptosis plays a key role in the regulation of normal renal structure and kidney remodeling in various renal diseases. Angiotensin II plays a prominent role in renal injury through its receptor subtypes, the type 1 (AT1) receptor and the type 2 (AT2) receptor, which involve different molecular mechanisms. In addition to its haemodynamic actions, angiotensin II induces apoptosis. Angiotensin II also increases proliferation in the kidney. A close correlation between renal cell proliferation and apoptosis has been shown in renal diseases as well as in the angiotensin II infusion model. Angiotensin induces upregulation of p53 and other pro-apoptotic proteins. Recent studies suggest that both AT1 and AT2 receptors influence the apoptotic process in the kidney. These apoptotic effects of angiotensin II should be considered as representing another regulatory mechanism that may modulate the balance between cell growth and proliferation within the kidney.
Gov't Doc #: 11549846
URI: https://ahro.austin.org.au/austinjspui/handle/1/9339
DOI: 52624
Journal: Experimental nephrology
URL: https://pubmed.ncbi.nlm.nih.gov/11549846
Type: Journal Article
Subjects: Angiotensin II.metabolism
Animals
Apoptosis.physiology
Cell Division.physiology
Kidney.cytology.physiology
Protein Isoforms
Receptors, Angiotensin.metabolism
Tumor Suppressor Protein p53.metabolism
Vasoconstrictor Agents.metabolism
Appears in Collections:Journal articles

Show full item record

Page view(s)

28
checked on Feb 22, 2025

Google ScholarTM

Check


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.