The common pathological pathway in progressive chronic kidney disease (CKD) is tissue fibrosis and chemokine receptor type 4 (CXCR4) plays a key role in the development of fibrosis.
Immunoglobulin A (IgA) nephropathy is the most prevalent glomerulonephritis worldwide that does not have a specific treatment. Its pathogenesis is complex and not well understood, but there is increasing evidence that the lectin-driven complement activation may be behind it. Mannose-binding lectin serine protease 2 (MASP-2) has been studied as a therapeutic target in the treatment of IgA nephropathy, as it is one of the main lectin pathway activators.
Congenital anomalies of the kidneys and urinary tract (CAKUT) remain the main cause of chronic kidney disease before the age of 25 years, and account for about 40% of childhood end-stage renal diseases. Studies in Xenopus species have shown ENPP6 knockdown to lead to impaired pronephros development, and mutations in the ENPP6 paralogue PIGN gene have been tied to CAKUT.
Protein tyrosine phosphatase 4A1 (PTP4A1) is known to promote tumor growth and migration of tumoral cells, but its role in the kidney has not been deeply explored. Researchers from Korea have aimed to investigate the role of PTP4A1 during kidney fibrosis and suggest it as a potential therapeutic target.
Nicorandil is a potent K(ATP) channel activator and a sulfonylurea receptor 2 (SUR2) selective agonist launched for the treatment of angina pectoris. Nicorandil binds to ATP-sensitive KATP channels in the mitochondrial inner membrane to preserve mitochondrial function during ischemia.
Medshine Discovery Inc. has divulged halogen-substituted pyridazinone compounds acting as short transient receptor potential channel 5 (TRPC5) antagonists reported to be useful for the treatment of hypertensive nephropathy.
A recent Shenzhen Salubris Pharmaceuticals Co. Ltd. patent describes prodrugs of atrasentan that act as endothelin ETA receptor antagonists. As such, they are reported to be useful for the treatment of chronic kidney disease, focal segmental glomerulosclerosis, hypertension and IgA nephropathy.
A study from the University Medical Center Hamburg-Eppendorf (UKE) in Germany has identified a type of T cell that triggered glomerulonephritis (GN) and produced loss of kidney function in mice. The scientists described an autoimmune pathway of this disease mediated by the accumulation of T cells producing granulocyte-macrophage colony-stimulating factor (GM-CSF) in the kidneys and found a possible therapeutic target.
Reduction of renal tubular cell polynucleotide phosphorylase (PNPT1) expression has been linked to renal tubular atrophy in chronic kidney disease, according to a new study. The research, published in Nature Communications, found that renal tubular cell PNPT1 reduction causes renal tubular atrophy by inhibiting protein synthesis.
A deficiency in fumarate metabolism could be behind a new mechanism of inflammation mediated by mitochondrial DNA and RNA. Two independent and simultaneous studies described how the accumulation of fumarate in the mitochondria released the genetic material of this organelle through vesicles, activating an inflammatory signaling pathway.
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