High Mobility Group Box 1 Promotes Aortic Calcification in Chronic Kidney Disease via the Wnt/β-Catenin Pathway.

Vascular calcification (VC) is common in chronic kidney disease (CKD), where cardiovascular mortality remains the leading cause of death. Here, we examined the role of high-mobility group box1 (HMGB1), a nuclear DNA-binding protein involved in inflammation, in aortic calcification and renal dysfunction induced by high phosphate in a mouse model of CKD induced by 5/6 nephrectomy. HMGB1 and kidney function markers were measured by ELISA in the serum of CKD patients and in CKD mice.

Downregulation of Syndecan-1 induce glomerular endothelial cell dysfunction through modulating internalization of VEGFR-2.

Ischemic acute kidney injury (AKI) remains to have high morbidity and mortality rates. The mechanism of glomerular endothelial cells (GEnC) dysfunction in the development of ischemic AKI is still unclear. Syndecan-1, one kind of heparan sulfate proteoglycan (HSPG), is extensively studied in tumor for its effects in promoting angiogenesis.

Down-regulation of Wt1 activates Wnt/β-catenin signaling through modulating endocytic route of LRP6 in podocyte dysfunction in vitro.

Podocyte dysfunction plays important roles in the pathogenesis of chronic kidney disease, and Wt1 has long been considered to be a marker of podocyte, whereas its roles and mechanisms in podocyte injury are still unclear though Wt1 mutations are reported to be involved in the development of glomerular disease in human and mice. Here we show that down-regulation of Wt1 could induce podocyte dysfunction and apoptosis through activating Wnt/β-catenin signaling. Podocytes treated with adriamycin demonstrated decreased expression of Wt1, coupled with activated Wnt/β-catenin signaling in vitro.

Neutrophil gelatinase-associated lipocalin (NGAL) may play a protective role against rats ischemia/reperfusion renal injury via inhibiting tubular epithelial cell apoptosis.

We investigated the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) on rats ischemia/reperfusion (I/R) renal injury. Eighteen Sprague-Dawley male rats were randomly divided into three groups. Control group (n = 6) suffered left unilateral nephrectomy, I/R + NS (normal saline) (n = 6) and I/R + NGAL (n = 6) group were subjected to 45 min right renal ischemia/24 h reperfusion after left unilateral nephrectomy.

Neutrophil gelatinase-associated lipocalin protects renal tubular epithelial cell in ischemic/reperfusion injury rats via apoptosis-regulating proteins.

We investigated the role of neutrophil gelatinase-associated lipocalin (NGAL) on renal tubular epithelial cell in the renal ischemia/reperfusion injury (IRI) rats. Male Sprague-Dawley rats were randomly assigned to three groups. The control group (n = 5) underwent left nephrectomy.