TGF-beta 1-induced epithelial-to-mesenchymal transition and therapeutic intervention in diabetic nephropathy [PDF]
, 2010 Background/Aims: Epithelial-to-mesenchymal cell transformation (EMT) is the trans-differentiation of tubular epithelial cells into myofibroblasts, an event underlying progressive chronic kidney disease in diabetes, resulting in fibrosis.
Hills, Claire E., Squires, Paul E.
core +1 more source
Activation of Rac-1 and RhoA contributes to podocyte injury in chronic kidney disease [PDF]
, 2013 Rho-family GTPases like RhoA and Rac-1 are potent regulators of cellular signaling that control gene expression, migration and inflammation. Activation of Rho-GTPases has been linked to podocyte dysfunction, a feature of chronic kidney diseases (CKD). We
Amann, Kerstin +13 more
core +4 more sources
Anti-glomerular basement membrane disease in HLA-identical non-twin siblings
Nefrología (English Edition), 2022 Anti glomerular basement membrane disease (AGBM) is an autoinmune disorder characterised by the presence of anti-glomerular basement membrane (Anti-GBM) antibodies, alveolar hemorrhage, necrotizing glomerulonephritis, and linear deposition of ...
Paz Castro Fernández +10 more
doaj +1 more source
Anti-glomerular Basement Membrane Disease with Antiphospholipid Syndrome
Internal Medicine, 2021 A 48-year-old woman presented with a fever, microscopic hematuria, proteinuria, and rapid deterioration of the renal function. Pulmonary alveolar hemorrhaging and a high level of anti-glomerular basement membrane (GBM) antibodies (700 IU/mL) were observed.
Torigoe, Miki +5 more
openaire +3 more sources
REGULATORY ROLE OF OX22HIGH T-CELLS IN MERCURY-INDUCED AUTOIMMUNITY IN THE BROWN NORWAY RAT [PDF]
, 1993 The monoclonal antibody OX22 defines a functional split within CD4+ T cells in the rat, with OX22high cells mainly producing interleukin 2 (IL-2) and interferon γ and responsible for delayed-type hypersensitivity responses, and OX22low cells mainly ...
Mathieson, PW, Oliveira, DB, Thiru, S
core +1 more source
Syndecan-4 knockout leads to reduced extracellular transglutaminase-2 and protects against tubulointerstitial fibrosis [PDF]
, 2013 Transglutaminase type 2 (TG2) is an extracellular matrix crosslinking enzyme with a pivotal role in kidney fibrosis. The interaction of TG2 with the heparan sulfate proteoglycan syndecan-4 (Sdc4) regulates the cell surface trafficking, localization, and ...
Burhan, I +6 more
core +1 more source
Anti-glomerular basement membrane disease associated with thin basement membrane nephropathy
Medicine, 2021 Abstract Rationale: Simultaneous occurrence of anti-glomerular basement membrane (anti-GBM) disease and thin basement membrane nephropathy (TBMN), both of which invade the type IV collagen subunits, is very rare. Here, we present the case of a 20-year-old male patient diagnosed with both anti-GBM disease and TBMN upon
Chi Young Jung +4 more
openaire +2 more sources
Monotypic IgG1-kappa Atypical Anti-Glomerular Basement Membrane Nephritis: A Case Report
Case Reports in Nephrology and Dialysis, 2019 Anti-glomerular basement membrane (anti-GBM) glomerulonephritis is a rare disease caused by autoantibodies against the glomerular basement membrane. Atypical anti-GBM nephritis is clinically less aggressive and characterized by the absence of circulating
Maxim Olivier +5 more
doaj +1 more source
Hyperfunctional complement C3 promotes C5-dependent atypical hemolytic uremic syndrome in mice [PDF]
, 2019 Atypical hemolytic uremic syndrome (aHUS) is frequently associated in humans with loss-of-function mutations in complement-regulating proteins or gain-of-function mutations in complement-activating proteins.
Atkinson, John P +11 more
core +3 more sources
Pembrolizumab-Induced Anti-GBM Glomerulonephritis: A Case Report
Kidney Medicine, 2023 Immune checkpoint inhibitors are known to have a wide range of autoimmune toxicities, such as acute interstitial nephritis. Immunotherapy induced glomerulonephritis has been described, but anti-glomerular basement membrane disease (anti-GBM) is rarely ...
Nidal El Yamani +6 more
doaj +1 more source