Nosirudeen Quadri

TL;DR: Inhibition of glutaminolysis, the essential component of ferroptosis, can reduce heart injury triggered by ischemia/reperfusion, suggesting a potential therapeutic approach for treating related diseases.

TL;DR: Deletion of RAGE in OVE26 mice reduced nephromegaly, mesangial sclerosis, cast formation, glomerular basement membrane thickening, podocyte effacement, and albuminuria, providing compelling evidence for critical roles for Rages in the pathogenesis of diabetic nephropathy and suggest that strategies targeting Rage in long-term diabetes may prevent loss of renal function.

TL;DR: NMR spectroscopy and x-ray crystallization studies of the extracellular domains of RAGE indicate that RAGE ligands bind by distinct charge- and hydrophobicity-dependent mechanisms, and provide support for the feasibility of inhibition of protein-protein interaction (PPI).

TL;DR: It is demonstrated that MPT pore opening is a key event by which AR pathway mediates myocardial I/R injury, and that the MPTpore opening after I-R is triggered, in part, by increases in ROS generation in ARTg mice hearts.

TL;DR: A novel role for AR is demonstrated in regulating the signaling pathways leading to neutrophil-EC adhesion during acute lung inflammation, and AR activity in both human neutrophils and ECs was required for neutrophIL adhesion to TNF-α-stimulated ECs.