As PGC-1α is well-established to mediate mitochondrial biogenesis and metabolic stress adaptation in other cell types6, we examined PGC-1α expression in endothelial cells from wild-type (WT) mice treated with a pressor dose (i.e, a dose known to induce endothelial dysfunction in WT mice) of angiotensin II (ATII). Here, PPARGC1A is linked to endothelial dysfunction.