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Podocyte-Specific Loss of Krüppel-Like Factor 6 Increases Mitochondrial Injury in Diabetic Kidney Disease.

Silence of IGFBP7 suppresses apoptosis and epithelial mesenchymal transformation of high glucose induced-podocytes.

Activation of mineralocorticoid receptor by ecdysone, an adaptogenic and anabolic ecdysteroid, promotes glomerular injury and proteinuria involving overactive GSK3β pathway signaling.

MAGI-2 and scaffold proteins in glomerulopathy.

Therapeutic potential of stromal cells of non-renal or renal origin in experimental chronic kidney disease.

Overexpression of KLF5 inhibits puromycin‑induced apoptosis of podocytes.

Induced pluripotent stem cell derived podocyte like cells as models for assessing mechanisms underlying heritable disease phenotype: initial studies using two Alport syndrome patient lines indicate impaired potassium channel activity.

Endoplasmic reticulum stress and monogenic kidney diseases in precision nephrology.

A pan-NADPH Oxidase Inhibitor Ameliorates Kidney Injury in Type 1 Diabetic Rats.

Solution Fibre Spinning Technique for the Fabrication of Tuneable Decellularised Matrix-Laden Fibres and Fibrous Micromembranes.

miR-370 promotes high glucose-induced podocyte injuries by inhibiting angiotensin II type 1 receptor-associated protein.

SGLT2 inhibitor dapagliflozin limits podocyte damage in proteinuric nondiabetic nephropathy.

Elucidation of Critical Epitope of Anti-Rat Podoplanin Monoclonal Antibody PMab-2.

Drosophila renal system as an in-vivo tool for target identification and screening of potential therapeutics for the diabetic nephropathy.

Angiotensin II Modulates Podocyte Glucose Transport.

Understanding Podocyte Biology to Develop Novel Kidney Therapeutics.

Niclosamide ethanolamine improves kidney injury in db/db mice.

Mutations in WDR4 as a new cause of Galloway-Mowat syndrome.

TRPC6-Mediated Ca2+ Signaling is Required for Hypoxia-Induced Autophagy in Human Podocytes.

Inhibition of pannexin-1 channel activity by adiponectin in podocytes: Role of acid ceramidase activation.

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