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7273件中 121件~140件表示    検索結果をPubMedで見る PubMedで見る

The protective effects of rapamycin on cell autophagy in the renal tissues of rats with diabetic nephropathy via mTOR-S6K1-LC3II signaling pathway.

Extracorporeal Stromal Cell Therapy for Subjects With Dialysis-Dependent Acute Kidney Injury.

Glomeruli from patients with nephrin mutations show increased number of ciliated and poorly differentiated podocytes.

[Pathogenic Mechanisms of the Focal Segmental Glomerulosclerosis and Its Role in the Progression of IgA Nephropathy].

Plectin protects podocytes from adriamycin-induced apoptosis and F-actin cytoskeletal disruption through the integrin α6β4/FAK/p38 MAPK pathway.

Resveratrol ameliorates podocyte damage in diabetic mice via SIRT1/PGC-1α mediated attenuation of mitochondrial oxidative stress.

Triptolide protects podocytes via autophagy in immunoglobulin A nephropathy.

REVERSAL OF ALBUMINURIA BY COMBINED AM6545 AND PERINDOPRIL THERAPY IN EXPERIMENTAL DIABETIC NEPHROPATHY.

Mutations in multiple components of the nuclear pore complex cause nephrotic syndrome.

Elevated aerobic glycolysis in renal tubular epithelial cells influences the proliferation and differentiation of podocytes and promotes renal interstitial fibrosis.

Triptolide, A Potential Autophagy Modulator.

Role of Mesangial-Podocytic-Tubular Cross-Talk in IgA Nephropathy.

Febrile Proteinuria in Hospitalized Children: Characterization of Urinary Proteins.

Organoids from Nephrotic Disease-Derived iPSCs Identify Impaired NEPHRIN Localization and Slit Diaphragm Formation in Kidney Podocytes.

MiR-874 alleviates renal injury and inflammatory response in diabetic nephropathy through targeting toll-like receptor-4.

Human Pluripotent Stem Cell Derived Kidney Model for Nephrotoxicity Studies.

An adjustment in BMP4 function represents a treatment for diabetic nephropathy and podocyte injury.

Glomerular endothelial cells versus podocytes as the cellular target in diabetic nephropathy.

Mucin-1 Gene Mutation and the Kidney: The Link between Autosomal Dominant Tubulointerstitial Kidney Disease and Focal and Segmental Glomerulosclerosis.

Nuclear YAP localization as a key regulator of podocyte function.

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