Interaction of PGC-1α and GDF15 in the stressed heart

Abstract

Upregulation of PGC-1α in the mouse heart during exercise training maintains mitochondrial homeostasis and promotes physiological hypertrophy by suppressing the stress-induced production of GDF15 in cardiomyocytes independently of its circulating levels. Identification of this cell-autonomous signaling circuit provides novel insights into the functional role of GDF15 in health and diseases. Future studies are warranted to investigate the interaction of PGC-1α and GDF15 in other stress conditions and in human subjects.