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. 2019 May 22;317(2):C209–C225. doi: 10.1152/ajpcell.00538.2018

Fig. 10.

Fig. 10.

Schematic diagram showing the role of APOL1 risk alleles in blockade autophagy in podocytes. APOL1G1 and APOL1G2 enhance expression of Rubicon, which forms a Rubicon complex inhibiting phosphorylation of UVRAG and attenuates generation of PI3P, resulting in inhibition of fusion of autophagosomes with lysosomes. Disruption of APOL1-miR193a axis in APOL1 risk milieu enhances expression of miR193a. miR193a attenuates transcription of PIK3C3′s regulatory unit (PIK3R3) and compromises maturation of autophagosomes. miR193a-induced attenuated transcription of mTOR is inhibiting the reformation of lysosomes required for fusion with autophagosomes. APOL1, apolipoprotein L1; PI3P, phosphatidyinositol-3-phosphate; PI3K, phosphatidylinositol 3-kinase; Pi3KC3, class III phosphatidylinositol 3-kinase; PIK3E3, PI3KC3′s regulatory unit; mTOR, mammalian target of rapamycin; Rubicon, run domain beclin-1-interacting and cysteine-rich domain-containing protein; UVRAG, UV radiation resistance-associated gene.