The novel mitochondrial microprotein PUTZ is a potential therapeutic target for aging-associated sarcopenia and frailty
Skeletal muscle is not only a locomotive tissue but also an endocrine organ, and age-associated skeletal muscle atrophy (i.e., sarcopenia and frailty) increases the risks of morbidity and mortality. Dr. Kumagai’s team recently discovered a novel mitochondrial-derived microprotein, a small-sized protein that has not been identified in the Human Genome Project, which regulates skeletal muscle function. Administration of this microprotein into mice causes skeletal muscle wasting and weakness. However, the details about this microprotein have not been clarified yet. Thus, the goal of this AFAR-supported project is to understand the mechanisms of how this microprotein causes skeletal muscle dysfunction and to find a way to suppress the bioactivity of this microprotein. The findings gained from this work will help establish a therapeutic approach against aging-related sarcopenia and frailty.
