Lithium-induced apoptotic cell death is not accompanied by a noticeable inflammatory response in the kidney.

Lithium (Li) therapy is a valuable tool in psychiatric practice that remains underutilized due to safety concerns. Excessive plasma Li levels are nephrotoxic and can trigger a local immune response. Our understanding of the immunomodulatory effects of Li in the kidney is fragmentary.

Aldosterone Antagonism Is More Effective at Reducing Blood Pressure and Excessive Renal ENaC Activity in AngII-Infused Female Rats Than in Males.

Background: AngII (angiotensin II)-dependent hypertension causes comparable elevations of blood pressure (BP), aldosterone levels, and renal ENaC (epithelial Na channel) activity in male and female rodents. Mineralocorticoid receptor (MR) antagonism has a limited antihypertensive effect associated with insufficient suppression of renal ENaC in male rodents with AngII-hypertension. While MR blockade effectively reduces BP in female mice with salt-sensitive and leptin-induced hypertension, MR antagonism has not been studied in female rodents with AngII-hypertension.

Evaluating Mechanisms of IDH1 Regulation through Site-Specific Acetylation Mimics.

Isocitrate dehydrogenase (IDH1) catalyzes the reversible NADP-dependent oxidation of isocitrate to α-ketoglutarate (αKG). IDH1 mutations, primarily R132H, drive > 80% of low-grade gliomas and secondary glioblastomas and facilitate the NADPH-dependent reduction of αKG to the oncometabolite D-2-hydroxyglutarate (D2HG). While the biochemical features of human WT and mutant IDH1 catalysis have been well-established, considerably less is known about mechanisms of regulation.