Engineered mesenchymal stem cells (MSCs) could produce mutant β-galactosidase and trigger nitric oxide (NO) release when the NO prodrug is systemically administered, which can achieve NO release in a precise spatiotemporal manner and augment the therapeutic efficiency of MSCs.

An unbiased approach unveils a non-canonical substrate of the known transporters, highlighting the mechanism behind the use of D-serine as a kidney biomarker.

Single-nuclear transcriptomic profiling and functional assays identified PKR activation and mitochondrial dysfunction in HIV-associated nephropathy mice kidneys.

Single-cell RNA-sequencing identifies the precise cellular and molecular events that occur along the sepsis timeline in the kidney, pointing to potential biomarkers and therapeutic targets.

Illustrating the impact of host metabolism on infection outcome, loss of the aryl hydrocarbon receptor in radioresistant cells leads to heme-mediated kidney toxicity during malaria.

PSTPIP2 reduced IL-19 secretion by inhibiting activation of the NF-κB pathway in renal tubular epithelial cells (RTECs), reducing the generation of neutrophil extracellular trap, which can participate in both aristolochic acid I-induced renal injury and apoptosis in RTECs.

Ferroptotic stress enhances the accumulation of damage-associated inflammatory proximal tubular cell state, thereby promoting maladaptive renal repair and the AKI-to-CKD transition.

Renal capillary pericytes are a novel therapeutic target for reducing sustained reduction in renal blood flow ('no-reflow') after kidney ischaemia.

Fundc1-mediated mitophagy protects renal EPO-producing cells from myofibroblastic conversion under stresses.

The repression of HIF-1 plays a central role in mitochondrial reactive oxygen species (ROS) overproduction and subsequent tissue damage in diabetes, which is mediated by increased mitochondrial respiration, making HIF-1 signaling an attractive therapeutic target for diabetes complications.