During nephron regeneration, renal interstitial cells promote the proliferation of renal progenitor cells by secreting PGE2, thus forming the microenvironment of renal progenitor cells.

The ability of the adult zebrafish to replace damaged nephrons in the kidney depends on renal progenitor cells and renal interstitial cells working closely together.

Assessing metabolites in renal cell carcinoma and kidney tissue suggests cancers adapt rather than dictate nutrient availability.

Genetic and chemical genetic analysis pinpoint defective epithelial cells as the driver for NPHP like phenotypes in Invs mutants, demonstrate genetic interaction between Invs and Ift88 and identify the HDAC inhibitor valproic acid as a suppressor for Invs mutant phenotypes.

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

Three-dimensional imaging was used to identify structural and quantitative features of developing lymphatics in the kidneys of mice, humans and in a genetic mouse model of polycystic kidney disease.

The neutral amino acid transporter SLC38A2 is an essential protective factor for renal medulla during urine concentration.

The use of multi-chemokine receptor reporter mice helps to unravel the dynamics of receptor involvement in leukocyte migration in vivo and suggests specificity, rather than redundancy, in receptor use.

Oxidized LDL synergizes with angiotensin II to amplify Gq signaling via the AT1-LOX1 receptor complex, revealing a novel mechanism driving renal dysfunction in hypertension and dyslipidemia.

Lymphangiogenic therapy VEGFCc156s improved angiotensin-II-induced impairments in heart function via novel mechanisms, which include transcriptional responses to alleviate inflammation and cardiac fibrosis, and systemic responses to ameliorate hypertension.