gene deficiency accelerates unilateral ureteral obstruction-induced kidney inflammation through oxidative stress and activation of macrophages.

Mitochondrial NADP-dependent isocitrate dehydrogenase 2 () produces NADPH, which is known to inhibit mitochondrial oxidative stress. Ureteral obstruction induces kidney inflammation and fibrosis oxidative stress. Here, we investigated the role and underlying mechanism of in unilateral ureteral obstruction (UUO)-induced kidney inflammation using gene deleted mice (). Eight- to 10-week-old female mice and wild type () littermates were subjected to UUO and kidneys were harvested 5 days after UUO. was not detected in the kidneys of mice, while UUO decreased in mice. UUO increased the expressions of markers of oxidative stress in both and mice, and these changes were greater in mice compared to mice. Bone marrow-derived macrophages of mice showed a more migrating phenotype with greater ruffle formation and Rac1 distribution than that of mice. Correspondently, UUO-induced infiltration of monocytes/macrophages was greater in mice compared to mice. Taken together, these data demonstrate that plays a protective role against UUO-induced inflammation through inhibition of oxidative stress and macrophage infiltration.