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A look at transactivation of the EGF receptor by angiotensin II.

A growing number of clinical and experimental studies show that the renin–angiotensin system (RAS) is involved in the progression of CKD.1 In fact, pharmacological inhibitors of the RAS such as angiotensin-converting enzyme inhibitors and angiotensin II (Ang II) type I receptor (AT1R) blockers are the most reliable and effective tools known to attenuate progression of parenchymal changes in CKD.1 However, despite the clinical evidence, understanding how RAS inhibition exerts its renoprotective function at the molecular level remains unclear.