Symmetric dimethylarginine (SDMA) is one of the byproducts of protein methylation, and it has been previously identified as an independent cardiovascular risk factor in patients with chronic kidney disease. The majority of SDMA is excreted through renal tubules; however, its effect on kidney in pathological conditions is not fully understood. In a recent study, researchers from Shuguang Hospital aimed to investigate the role of SDMA in renal tubulointerstitial fibrosis.
Rona Therapeutics Inc. and Keymed Biosciences Co. Ltd. have established a collaboration to jointly discover and develop first-in-class siRNA therapeutics for glomerulonephritis. The collaboration will leverage both companies’ scientific and technological expertise and will build on Rona’s proprietary platform in RNAi targeting liver and extrahepatic tissues.
The limited state of current clinical transplantation science was recently the subject of an opinion piece from an individual that received her first heart transplant at just 25 years of age only to soon succumb at the age of 60 to one of the many risky outcomes expected for anyone taking standard requisite immunosuppression regimens used for any transplantation, in her case terminal cancer.
Long Island University and Mount Sinai School of Medicine have jointly developed intermediate conductance KCa3.1 (IKCa1) channel blockers reported to be useful for the treatment of renal disorders.
A recent study investigated the role of neuraminidase 1 (NEU1) in renal fibrosis. Researchers found increased levels of NEU1 in the fibrotic kidneys of patients and two mouse models of renal fibrosis (mice subjected to unilateral ureteral obstruction or administered folic acid).
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.
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