Multimodal Action of Mas Activation for Systemic Cancer Cachexia Therapy.

Abstract

Cancer cachexia remains a largely intractable, deadly condition for patients with no approved, effective therapies. However, research progress over the past few decades demonstrates that cachexia is a disease with specific, targetable mechanisms. New work by Murphy and colleagues in this issue of <i>Cancer Research</i> suggests that activation of the alternative renin-angiotensin system with the nonpeptide Mas receptor agonist AVE 0991 holds promise for reducing muscle wasting in cancer. Their cell studies demonstrate on-target activity in skeletal muscle cells, whereas their mouse results suggest potentially more important systemic effects.<i>See related article by Murphy et al., p. 706</i>.