Yanhong Ma

TL;DR: PGC-1α and ERR-α, major regulators of mitochondrial function in response to exercise and other stimuli, also control a novel angiogenic pathway that delivers needed oxygen and substrates, and may provide a novel therapeutic target for treating ischaemic diseases.

TL;DR: It is shown that transgenic expression of PGC-1beta causes a marked induction of IIX fibers, which are oxidative but have "fast-twitch" biophysical properties and are rich in mitochondria and are highly oxidative, at least in part due to coactivation by P GC-1 beta of ERRalpha and PPARalpha.

TL;DR: It is shown that TAC in mice genetically engineered to lack PGC-1alpha leads to accelerated cardiac dysfunction, which is accompanied by signs of significant clinical heart failure, and the data suggest that elevating P GC-1 alpha activity may have therapeutic potential in the treatment of heart failure.

TL;DR: A high-throughput screen to identify small molecules that induce PGC-1α expression in skeletal muscle cells is described, and microtubule inhibitors and protein synthesis inhibitors are identified as modulators of P GC-1 α and oxidative phosphorylation.

TL;DR: Metabotropic glutamate receptor 5 blockade using MTEP ameliorates PAH‐induced pathological right cardiac remodelling via inhibiting the signalling cascade involving PI3K/AKT, P38MAPK, Ang 2 and VEGF.