TY - JOUR
T1 - Angiotensin II and growth factors in the pathogenesis of diabetic nephropathy
AU - Rincon-Choles, Hernan
AU - Kasinath, Balakuntalam S.
AU - Gorin, Yves
AU - Abboud, Hanna E.
N1 - Funding Information:
Dr. H. Rincon-Choles is an Associate Investigator Awardee funded by the Research Enhancement Award Program (REAP) from the Veterans Administration. Dr. Y. Gorin was supported by the NKF Texas Affiliate. Drs. H.E. Abboud and B.S. Kasinath are funded by NIH, VA and ADA.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2002
Y1 - 2002
N2 - The renin-angiotensin system (RAS) and growth factors mediate structural and functional changes during the course of diabetic nephropathy (DN). Studies in humans and experimental models with DN suggest their involvement in the development and progression of DN. Activation of renal tissue RAS and increased expression of growth factors have been demonstrated at early stages of the disease. Angiotensin II and growth factors alter renal hemodynamics and exert trophic changes in renal cells that eventually result in fibrosis through direct mechanisms or through the release of other mediators. Their effects are likely modulated by metabolic changes including high glucose and free fatty acids. While blockade of the RAS ameliorates DN in humans, such evidence for blockade of growth factors is still lacking. It is likely that susceptibility to the development of DN and therapeutic efficacy are modulated by genetic polymorphisms in components of the RAS and growth factors including their receptors and other target molecules. Approaches to understand the intricate relationship between these systems and the mechanism(s) by which they alter capillary permeability and result in structural changes are areas of fruitful investigation.
AB - The renin-angiotensin system (RAS) and growth factors mediate structural and functional changes during the course of diabetic nephropathy (DN). Studies in humans and experimental models with DN suggest their involvement in the development and progression of DN. Activation of renal tissue RAS and increased expression of growth factors have been demonstrated at early stages of the disease. Angiotensin II and growth factors alter renal hemodynamics and exert trophic changes in renal cells that eventually result in fibrosis through direct mechanisms or through the release of other mediators. Their effects are likely modulated by metabolic changes including high glucose and free fatty acids. While blockade of the RAS ameliorates DN in humans, such evidence for blockade of growth factors is still lacking. It is likely that susceptibility to the development of DN and therapeutic efficacy are modulated by genetic polymorphisms in components of the RAS and growth factors including their receptors and other target molecules. Approaches to understand the intricate relationship between these systems and the mechanism(s) by which they alter capillary permeability and result in structural changes are areas of fruitful investigation.
KW - AGEs
KW - Capillary permeability
KW - Fibrosis
KW - Hemodynamics
KW - Progressive renal disease
KW - Renin-angiotensin system
KW - Transforming growth factor-β
UR - http://www.scopus.com/inward/record.url?scp=0036435877&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036435877&partnerID=8YFLogxK
U2 - 10.1046/j.1523-1755.62.s82.3.x
DO - 10.1046/j.1523-1755.62.s82.3.x
M3 - Article
C2 - 12410848
AN - SCOPUS:0036435877
VL - 62
SP - S8-S11
JO - Kidney International, Supplement
JF - Kidney International, Supplement
SN - 0098-6577
IS - 82
ER -