In their most recent study appearing in the Journal of Clinical Investigation, these same authors used a variety of techniques to demonstrate that angiotensin II inhibits IGF-1 signaling in skeletal muscle and that this effect is causally related to skeletal muscle loss. They also demonstrate that in mice genetically engineered to overproduce IGF-1 there is a complete reversal of angiotensin-induced weight loss. The authors provide strong evidence that the signaling pathway known as the Akt/mTOR/p70S6 kinase pathway is involved in this ability of IGF-1 to prevent muscle loss.
These findings have broad relevance to the events leading to muscle loss in a variety of conditions such as chronic congestive heart failure and chronic renal failure. In addition, the study provides a strong rationale for developing strategies to activate the skeletal muscle IGF-1 system in wasting conditions for therapeutic benefit.
TITLE: Muscle-specific expression of IGF-1 blocks angiotensin II–induced skeletal muscle wasting.
AUTHOR CONTACT:
Patrick Delafontaine
Tulane University School of Medicine, New Orleans, Louisiana, USA.
Phone: 504-587-2025; Fax: 504-587-4237; E-mail: pdelafon@tulane.edu.
This article is available at: http://www.jci.org/papbyrecent.shtml.
Journal
Journal of Clinical Investigation