Key result
Angiotensin II is a potent inducer of TGF-beta synthesis in vitro, exerting biological effects such as extracellular matrix accumulation independently of its vasoconstrictive properties.
Angiotensin II may contribute to glomerulosclerosis by inducing TGF-beta synthesis independently of its hemodynamic effects, highlighting a potential therapeutic target for ACE inhibitors and ARBs.
In vitro Ang II–TGF-beta effects suggest non-hemodynamic fibrosis pathways; leaves open clinical translation to ACEi/ARB benefits in glomerulosclerosis.
Both angiotensin II and TGF-beta are key mediators of glomerular and tubulointerstitial injury and fibrosis in progressive kidney diseases. It was thought that angiotensin II damages the kidney by increasing glomerular filtration pressure, whereas autocrine TGF-beta overexpression occurs from unidentified mechanisms. Recent studies reveal that angiotensin II is a potent inducer of TGF-beta synthesis in a variety of cells and that this mechanism exerts important biological effects including extracellular matrix accumulation, cell proliferation, and hypertrophy. Because these studies were performed in vitro, there is clear evidence that the biological effects were observed independently of the vasoconstrictive properties of angiotensin II. Although it is difficult to study angiotensin II-mediated effects in vivo without influencing systemic and glomerular blood pressure, further studies are needed to evaluate the ability of ACE-inhibitors and angiotensin II receptor blockers to suppress TGF-beta overexpression in selected models of chronic progressive kidney disease.
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Ketteler et al. (1995) conducted a review in Progressive kidney diseases. Angiotensin II is a potent inducer of TGF-beta synthesis in vitro, exerting biological effects such as extracellular matrix accumulation independently of its vasoconstrictive properties.
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