Oxidative phosphorylation in kidney collecting duct is dispensable for maintaining water homeostasis at baseline, but necessary for maximal stimulation of AQP2 expression and urinary concentration.

HIF-PHIs for the prevention of bladder injury.

HIF-PHIs in CKD anemia: Regulation of EPO synthesis.

Disruption of mitochondrial complex III in cap mesenchyme but not in ureteric progenitors results in defective nephrogenesis associated with amino acid deficiency.

The studies provide mechanistic insights into dose-dependent effects of short-term pharmacologic HIF activation on renal hemodynamics, glomerular filtration and O2 metabolism and identify NO as a major mediator of these effects.

Kidney epithelial targeted mitochondrial transcription factor A deficiency results in progressive mitochondrial depletion associated with severe cystic disease.

Inactivation of HIF-prolyl 4-hydroxylases 1, 2 and 3 in NG2-expressing cells induces HIF2-mediated neurovascular expansion independently of erythropoietin.

Hypoxia-inducible factor prolyl-4-hydroxylation in FOXD1 lineage cells is essential for normal kidney development.

Distinct subpopulations of FOXD1 stroma-derived cells regulate renal erythropoietin.

Renal epithelium regulates erythropoiesis via HIF-dependent suppression of erythropoietin.

Prolyl-4-hydroxylase 2 and 3 coregulate murine erythropoietin in brain pericytes.