Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction

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Autophagy Regulates TGF-  Expression and Suppresses Kidney Fibrosis Induced by Unilateral Ureteral Obstruction

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Lysophosphatidic Acid Increases Proximal Tubule Cell Secretion of Profibrotic Cytokines PDGF-B and CTGF through LPA2- and Gαq-Mediated Rho and αvβ6 Integrin-Dependent Activation of TGF-β

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Autophagy Promotes Intracellular Degradation of Type I Collagen Induced by Transforming Growth Factor (TGF)-β1

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Autophagy Is a Renoprotective Mechanism During in Vitro Hypoxia and in Vivo Ischemia-Reperfusion Injury

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Tubular Overexpression of Transforming Growth Factor-β1 Induces Autophagy and Fibrosis but Not Mesenchymal Transition of Renal Epithelial Cells

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TGF-β1 Protects against Mesangial Cell Apoptosis via Induction of Autophagy

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Methylation determines fibroblast activation and fibrogenesis in the kidney

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Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury

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Inhibition of Autoregulated TGFβ Signaling Simultaneously Enhances Proliferation and Differentiation of Kidney Epithelium and Promotes Repair Following Renal Ischemia

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Mitochondrial Autophagy Is an HIF-1-dependent Adaptive Metabolic Response to Hypoxia

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Autophagy is cytoprotective during cisplatin injury of renal proximal tubular cells

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Autophagy fights disease through cellular self-digestion

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