What reflexively comes to mind when over-activation of the renin-angiotensin system (RAS) and the resultant elevated angiotensin-II levels are mentioned is hypertension, for which angiotensin-converting enzyme (ACE) inhibitors and angiotensin-II type 1 (ATI) receptor antagonists are the pharmacological therapy of choice. But the same situation exists in cachexia: angiotensin-II activates the ubiquitin-proteasome system via generation of reactive oxygen species and via inhibition of the insulin-like growth factor-1 signaling pathway [1,2].
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