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Effectiveness of a Novel PLA2R1 Knock-In Rat Model in Repairing Renal Function Damage.
J Biochem Mol Toxicol
January 2025
Shanxi Genetic Engineering Center for Experimental Animal Models, The Fifth Hospital (Shanxi Provincial People's Hospital) of Shanxi Medical University, Taiyuan, Shanxi, China.
Phospholipase A2 receptor 1 (PLA2R1) exists in many animals and plays an important role in membranous nephropathy. In this study, we aimed to evaluate a PLA2R1 knock-in rat model with repaired kidney function to study the molecular mechanisms of membranous nephropathy. We constructed the PLA2R1 knockout [PLA2R1(-)] model and PLA2R1 knock in [PLA2R1(+)] model in rats.
View Article and Find Full Text PDFBackground: The recurrence of primary glomerulonephritis (GN) following kidney transplantation poses a significant threat to graft survival. To enhance kidney transplant outcomes, we must lessen the burden of recurrence. In recent years, there has been progress in understanding the incidence, risk factors for recurrence, pathophysiology, biomarkers, and therapeutics, making it worthwhile to conduct an update on primary glomerulonephritis that may recur following kidney transplantation.
View Article and Find Full Text PDFPhospholipase A2 receptor 1 (PLA2R1) exists important role in membranous nephropathy. In this study, we evaluate a PLA2R1 in a middle-aged rat model of renal function repair to further investigate the molecular mechanisms of membranous nephropathy. We analyzed the PLA2R1 knockout (KO) model and PLA2R1 knock in (KI) model in rats, extending the time to 85 weeks of age.
View Article and Find Full Text PDFDynll1-PI31 Interaction Enhances Proteolysis via the Proteasome, Representing a Novel Therapeutic Target for INF2-Related FSGS.
Kidney360
December 2024
Division of Nephrology, Stead Family Department of Pediatrics, Carver College of Medicine, the University of Iowa.
Background: The p.Arg218Gln (R218Q) mutation in the inverted formin 2 (INF2) gene causes podocytopathy prone to focal segmental glomerulosclerosis (FSGS). This mutation disrupts the ability of INF2 to sequester DYNLL1, thus promoting dynein-mediated mistrafficking of the slit diaphragm protein, nephrin, to proteolytic pathways.
View Article and Find Full Text PDFRenalase protects against podocyte injury by inhibiting oxidative stress and apoptosis in diabetic nephropathy.
Open Life Sci
November 2024
Department of Nephrology, Faculty of Kidney Diseases, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Diabetic nephropathy (DN) presents a significant public health challenge due to its high rate of incidence and severe health consequences. Renalase has been identified as having renal-protective properties. A key contributor to albuminuria in DN patients is podocyte loss.
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