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.
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In vitro Ang II–TGF-beta effects suggest non-hemodynamic fibrosis pathways; leaves open clinical translation to ACEi/ARB benefits in glomerulosclerosis.
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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