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Urinary podocalyxin as a possible novel marker of intrauterine nephrogenesis and extrauterine podocyte injury.

Collapsing glomerulopathy, the Saudi Arabian scenario. A study of 31 cases and a review of literature.

Pyruvate kinase M2 activation may protect against the progression of diabetic glomerular pathology and mitochondrial dysfunction.

Natriuretic peptide receptor guanylyl cyclase-A pathway counteracts glomerular injury evoked by aldosterone through p38 mitogen-activated protein kinase inhibition.

A Personalized Model of COQ2 Nephropathy Rescued by the Wild-Type COQ2 Allele or Dietary Coenzyme Q10 Supplementation.

Deletion of Inositol-Requiring Enzyme-1α in Podocytes Disrupts Glomerular Capillary Integrity and Autophagy.

Rapamycin Induces Autophagy and Reduces the Apoptosis of Podocytes Under a Stimulated Condition of Immunoglobulin A Nephropathy.

Janus Kinase 2 Regulates Transcription Factor EB Expression and Autophagy Completion in Glomerular Podocytes.

Thrombin-Induced Podocyte Injury Is Protease-Activated Receptor Dependent.

Differential expression profile analysis of PSTK-regulated mRNAs in podocytes.

Urinary podocyte and TGF-β1 mRNA as markers for disease activity and progression in anti-glomerular basement membrane nephritis.

A disease model of diabetic nephropathy in a glomerulus-on-a-chip microdevice.

Cyclosporine A alters expression of renal microRNAs: New insights into calcineurin inhibitor nephrotoxicity.

Molecular mechanisms involved in podocyte EMT and concomitant diabetic kidney diseases: an update.

Metabolism and homeostasis in the kidney: metabolic regulation through insulin signaling in the kidney.

Effect of berberine on the renal tubular epithelial-to-mesenchymal transition by inhibition of the Notch/snail pathway in diabetic nephropathy model KKAy mice.

Activated protein C inhibits neutrophil extracellular trap formation in vitro and activation in vivo.

Novel Roles for Podocalyxin in Regulating Stress Myelopoiesis, Rap1a and Neutrophil Migration.

Fibrinogen links podocyte injury with Toll-like receptor 4 and is associated with disease activity in FSGS patients.

Focal segmental glomerulosclerosis and medullary nephrocalcinosis in children with ADCK4 mutations.

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