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. 2014 Jan 20;20(3):519–537. doi: 10.1089/ars.2013.5363

FIG. 7.

FIG. 7.

Autophagy in kidney diseases. (A) Activation of autophagy ameliorates DN. Autophagic activity is inhibited in DN due to aberrant energy sensing pathways. Reactivation of autophagy, for instance by caloric restriction, reduces oxidative stress and protects against DN. (B) Autophagy in PKD and NC is impaired. Basal level of autophagy can be altered through aberrant activation of mTOR or HIF-1α, and the autophagic flux is impaired in PKD. Whether autophagy protects against apoptosis in cyst lining tubular cells and cystogenesis is unknown. Mitophagy is impaired in NC through impairment of autophagic flux, and leads to tubular cell apoptosis, ROS production, and ATP reduction. (C) Autophagy can promote cell survival and tumor growth, or autophagic cell death in RCC. Loss of miR-204, through inactivation of VHL tumor suppressor gene, induces autophagy and tumor growth. In VHL-deficient RCC cells, STF-62247, or sphingosine kinase 2 inhibitor inhibits tumor growth through autophagic cell death. PI3K/mTOR inhibition induces apoptosis and autophagy. HIF-1α, hypoxia-inducible factor-1α; PI3K, phosphoinositide-3 kinase; PKD, polycystic kidney disease; VHL, von Hippel-Lindau; RCC, renal cell carcinoma; NC, nephropathic cystinosis; DN, diabetic nephropathy. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars

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