Podocyte specific knockout (KO) of the natriuretic peptide clearance receptor (NPRC) attenuates diabetic kidney disease (DKD). [PDF]
Abstract Glomerular podocytes play a key role in the pathogenesis of diabetic kidney disease (DKD). Recent studies suggest that natriuretic peptides (NPs) are podocyte protective. The beneficial effects of NPs are inhibited by the removal of NPs from the circulation by the NP clearance receptor (NPRC).
Wang L +4 more
europepmc +2 more sources
Urinary exosomes aggravate diabetic kidney disease by inducing podocyte ferroptosis via the miR-217/SIRT1/Nrf2 pathway. [PDF]
These findings indicate that urinary exosomal miR‐217 promotes podocyte ferroptosis and DKD progression via suppression of the SIRT1/Nrf2 pathway, suggesting a potential therapeutic target for DKD. Abstract Urinary exosomal microRNAs (miRNAs) mediate intercellular communication in diabetic kidney disease (DKD), a leading contributor to end‐stage renal ...
Du X +7 more
europepmc +2 more sources
Rap1 Activity Is Essential for Focal Adhesion and Slit Diaphragm Integrity
Glomerular podocytes build, with their intercellular junctions, part of the kidney filter. The podocyte cell adhesion protein, nephrin, is essential for developing and maintaining slit diaphragms as functional loss in humans results in heavy proteinuria.
Mee-Ling Maywald +9 more
doaj +1 more source
miR-135a-5p Is a Promising Target to Prevent the Glomerulosclerosis Associated with Podocyte Developmental Toxicity in Offspring Induced by Prenatal Dexamethasone Exposure. [PDF]
Prenatal dexamethasone exposure (PDE) programs persistent podocyte developmental injury and adult glomerulosclerosis. Mechanistically, glucocorticoid receptor (GR) binds the miR‐135a‐5p promoter and recruits the histone acetyltransferase p300, increasing promoter histone acetylation and sustaining miR‐135a‐5p expression. Elevated miR‐135a‐5p suppresses
Zhao X +8 more
europepmc +2 more sources
Multivalent nephrin–Nck interactions define a threshold for clustering and tyrosine-dependent nephrin endocytosis [PDF]
ABSTRACT Assembly of signaling molecules into micrometer-sized clusters is driven by multivalent protein-protein interactions, such as those found within the nephrin–Nck (Nck1 or Nck2) complex. Phosphorylation on multiple tyrosine residues within the tail of the nephrin transmembrane receptor induces recruitment of the cytoplasmic ...
Claire E. Martin +8 more
openaire +2 more sources
Glycosphingolipid GM3 prevents albuminuria and podocytopathy induced by anti-nephrin antibody
Podocytopathy, which is characterized by injury to podocytes, frequently causes proteinuria or nephrotic syndrome. There is currently a paucity of effective therapeutic drugs to treat proteinuric kidney disease.
Nagako Kawashima +8 more
doaj +1 more source
Podocytic PKC-alpha is regulated in murine and human diabetes and mediates nephrin endocytosis. [PDF]
BACKGROUND: Microalbuminuria is an early lesion during the development of diabetic nephropathy. The loss of high molecular weight proteins in the urine is usually associated with decreased expression of slit diaphragm proteins.
Irini Tossidou +9 more
doaj +1 more source
Urinary Nephrin and Podocalyxin Levels as Predictors of Pre-eclampsia in High-Risk Pregnant Women [PDF]
Introduction: Pre-eclampsia (PE) is characterized by new-onset hypertension and proteinuria. Damage of podocyte cells has been reported in pre-eclamptic women, thus podocyte specific proteins such as nephrin and podocalyxin could be useful biomarkers in ...
Irena Kostovska +3 more
doaj +3 more sources
Loss of S1P Lyase Expression in Human Podocytes Causes a Reduction in Nephrin Expression That Involves PKCδ Activation [PDF]
Sphingosine 1-phosphate (S1P) lyase (SPL, Sgpl1) is an ER-associated enzyme that irreversibly degrades the bioactive lipid, S1P, and thereby regulates multiple cellular functions attributed to S1P.
Imeri, Faik +11 more
core +1 more source
Expression Of Nephrin In Early Diagnosis Of Diabetic Nephropathy
Background & Objectives: Diabetic nephropathy occurs as a result of proximal tubule dysfunction with podocyte damage due to increased advanced glycation end-products’ insult in diabetes.
Moazzam A. Shahid +3 more
doaj +1 more source

