GDF11 mediates cardiac and skeletal muscle dysfunction and cachexia

Abstract

Growth differentiation factor 11 (GDF11) is important in regulating early fetal development of the axial skeleton and various visceral organs. Its actions on the adult body are less clear, and recent studies have led to conflicting accounts of GDF11’s ability to affect cardiac hypertrophy and skeletal muscle regeneration. If boosting GDF11 levels in adults had the ability to rejuvenate tissues and reverse the effects of aging, then the therapeutic possibilities are potentially vast. We attempted to provide clarification of this controversial topic by studying the effects of supraphysiologic levels of GDF11 in a mouse model using injected Chinese hamster ovary cells producing GDF11. We found that increasing endogenous levels of GDF11 in this in vivo mouse model resulted in overall bodily wasting, specifically with evidence of cardiac and skeletal muscle atrophy. In light of these results, caution must be exercised if GDF11 is ever considered as a potential therapeutic agent.