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tubular epithelial cells

Deletion of STAT3 from Foxd1 Cell Population Protects Mice from Kidney Fibrosis by Inhibiting Pericytes Trans-differentiation and Migration

[Cell Reports] Signal transduction and activator of transcription 3 (STAT3) activation increased migration and profibrotic signaling in genome-edited, pericyte-like cells. Conversely, blocking Stat3 inhibited detachment, migration, and profibrotic signaling.

The HDAC2/SP1/miR-205 Feedback Loop Contributes to Tubular Epithelial Cell Extracellular Matrix Production in Diabetic Kidney Disease

[Clinical Science] The authors described a novel feedback loop composed of histone deacetylase 2 (HDAC2) and miR-205 that regulated ECM production in tubular epithelial cells in individuals with diabetic kidney disease.

Tissue Culture Models of Acute Kidney Injury: From Tubule Cells to Human Kidney Organoids

[Journal of the American Society of Nephrology] Scientists explore the mechanisms and detection of acute kidney injury in tissue culture, with an emphasis on bioengineered approaches such as human kidney organoid models.

Lysine-Specific Demethylase 1 Induced Epithelial-Mesenchymal Transition and Promoted Renal Fibrosis through Jagged-1/Notch Signaling Pathway

[Human & Experimental Toxicology] Lysine-specific demethylase 1 significantly impacted on the progression of TGF-β1-mediated epithelial-mesenchymal transition and ECM deposition in HK-2 cells, and it may represent novel target for the prevention strategies of renal fibrosis.

CHIP-Overexpressing Wharton’s Jelly-Derived Mesenchymal Stem Cells Attenuate Hyperglycemia-Induced Oxidative Stress-Mediated Kidney Injuries in Diabetic Rats

[Free Radical Biology and Medicine] Western blot analysis, flow cytometry, and MitoSOX staining revealed that hyperglycemia-induced mitochondrial oxidative stress production and apoptosis were attenuated in CHIP-overexpressing Wharton's jelly-derived mesenchymal stem cells

Permissive Effect of GSK3β on Profibrogenic Plasticity of Renal Tubular Cells in Progressive Chronic Kidney Disease

[Cell Death & Disease] In vitro, TGF-β1 treatment augmented glycogen synthase kinase 3β expression in tubular epithelial cells, concomitant with dedifferentiation, cell cycle arrest at G2/M phase, excessive accumulation of extracellular matrix, and overproduction of profibrotic cytokines like PAI-1 and CTGF.

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