Research Perspective Volume 2, Issue 3 pp 170—176
MAP kinase phosphatase-1 - a new player at the nexus between sarcopenia and metabolic disease
- 1 Department of Pharmacology and Program in Integrative Cell Signaling and Neurobiology of Metabolism, Yale University School of Medicine, New Haven, CT 06520, USA
- 2 Current Address: Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Received: March 18, 2010 Accepted: April 1, 2010 Published: April 6, 2010https://doi.org/10.18632/aging.100135
How to Cite
Sarcopenia, which is defined by the loss of skeletal muscle mass, predisposes skeletal muscle to metabolic dysfunction which can precipitate metabolic disease. Similarly, overnutrition, which is a major health problem in modern society, also causes metabolic dysfunction in skeletal muscle and predisposition to metabolic disease. It is now the prevailing view that both aging and overnutrition negatively impact skeletal muscle metabolic homeostasis through deleterious effects on the mitochondria. Accordingly, interplay between the molecular pathways implicated in aging and overnutrition that induce mitochondrial dysfunction are apparent. Recent work from our laboratory has uncovered the stress-responsive mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) as a new player in the regulation of metabolic homeostasis in skeletal muscle and mitochondrial dysfunction caused by overnutrition. These observations raise the intriguing possibility that MKP-1 may function as a common target in the convergence between sarcopenia and overnutrition in a pathophysiological pathway that leads to a loss of skeletal muscle mitochondrial function. With the increasing aging population it will become more important to understand how MKP-1, and possibly other phosphatases, operate at the nexus between sarcopenia and metabolic disease.