Glenn C. Rowe

TL;DR: It is shown that BRAF inhibition also induces an oxidative phosphorylation gene program, mitochondrial biogenesis, and the increased expression of the mitochondrial master regulator, PGC1α, and a target of BRAF, the melanocyte lineage factor MITF, directly regulates the expression of P GC1α.

TL;DR: The data indicate that PPCM is mainly a vascular disease, caused by excess anti-angiogenic signalling in the peripartum period, and explain how late pregnancy poses a threat to cardiac homeostasis, and why pre-eclampsia and multiple gestation are important risk factors for the development of P PCM.

TL;DR: It is shown that endotoxemia reduces oxygen delivery to the kidney, without changing tissue oxygen levels, suggesting reduced oxygen consumption by the kidney cells, and that PGC-1α induction may be necessary for recovery from this disorder.

TL;DR: PPARGC1a is leveraged, a transcriptional coactivator that regulates broad programs of fatty acid consumption, to identify 3-hydroxyisobutyrate (3-HIB), a catabolic intermediate of the BCAA valine, as a new paracrine regulator of trans-endothelial fatty acid transport, providing a mechanistic explanation for how increased BCAA catabolic flux can cause diabetes.

TL;DR: Plasma metabolic profiles obtained during exercise provide signatures of exercise performance and cardiovascular disease susceptibility, in addition to highlighting molecular pathways that may modulate the salutary effects of exercise.