ArticleAmerican journal of physiology. Cell physiology2019
Disrupted apolipoprotein L1-miR193a axis dedifferentiates podocytes through autophagy blockade in an APOL1 risk milieu.
Article in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- The ATG14: multi-layer autophagy control and an emerging therapeutic target in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- HIV-1 Nef synergizes with APOL1-G1 to induce nephrocyte cell death in HIV-related kidney diseases.Disease models & mechanisms · 2025Article
- METTL10 attenuates adriamycin-induced podocyte injury by targeting cell dedifferentiation.Scientific reports · 2025Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Mechanisms and implications of podocyte autophagy in chronic kidney disease.American journal of physiology. Renal physiology · 2024Review
- Inspiring Tactics with the Improvement of Mitophagy and Redox Balance for the Development of Innovative Treatment against Polycystic Kidney Disease.Biomolecules · 2024Review
- APOL1-mediated monovalent cation transport contributes to APOL1-mediated podocytopathy in kidney disease.The Journal of clinical investigation · 2024Article
- Perturbations in podocyte transcriptome and biological pathways induced by FSGS associated circulating factors.Annals of translational medicine · 2023Article
- The Human Virome and Its Crosslink with Glomerulonephritis and IgA Nephropathy.International journal of molecular sciences · 2023Review
- Impaired autophagic flux and dedifferentiation in podocytes lacking Asah1 gene: Role of lysosomal TRPML1 channel.Biochimica et biophysica acta. Molecular cell research · 2023Article
- Transcriptomic Analysis of Human PodocytesKidney international reports · 2023Article
- A glomerular transcriptomic landscape of apolipoprotein L1 in Black patients with focal segmental glomerulosclerosis.Kidney international · 2022Article
- APOL1 risk variants and the development of HIV-associated nephropathy.The FEBS journal · 2021Review
- Article
- Collapsing Focal Segmental Glomerulosclerosis in Viral Infections.Frontiers in immunology · 2021Review
- The clinical significance of apolipoprotein L1 in head and neck squamous cell carcinoma.Oncology letters · 2020Article
- APOL1 polymorphism modulates sphingolipid profile of human podocytes.Glycoconjugate journal · 2020Article
- Autophagy in kidney homeostasis and disease.Nature reviews. Nephrology · 2020Review
- MiR193a Modulation and Podocyte Phenotype.Cells · 2020Article
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14 authors at 4 institutions in 4 countries.
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Abstract
We hypothesized that a functional apolipoprotein LI (APOL1)-miR193a axis (inverse relationship) preserves, but disruption alters, the podocyte molecular phenotype through the modulation of autophagy flux. Podocyte-expressing APOL1G0 (G0-podocytes) showed downregulation but podocyte-expressing APOL1G1 (G1-podocytes) and APOL1G2 (G2-podocytes) displayed enhanced miR193a expression. G0-, G1-, and G2-podocytes showed enhanced expression of light chain (LC) 3-II and beclin-1, but a disparate expression of p62 (low in wild-type but high in risk alleles). G0-podocytes showed enhanced, whereas G1- and G2-podocytes displayed decreased, phosphorylation of Unc-51-like autophagy-activating kinase (ULK)1 and class III phosphatidylinositol 3-kinase (PI3KC3). Podocytes overexpressing miR193a (miR193a-podocytes), G1, and G2 showed decreased transcription of PIK3R3 (PI3KC3's regulatory unit). Since 3-methyladenine (3-MA) enhanced miR193a expression but inhibited PIK3R3 transcription, it appears that 3-MA inhibits autophagy and induces podocyte dedifferentiation via miR193a generation. miR193a-, G1-, and G2-podocytes also showed decreased phosphorylation of mammalian target of rapamycin (mTOR) that could repress lysosome reformation. G1- and G2-podocytes showed enhanced expression of run domain beclin-1-interacting and cysteine-rich domain-containing protein (Rubicon); however, its silencing prevented their dedifferentiation. Docking, protein-protein interaction, and immunoprecipitation studies with antiautophagy-related gene (ATG)14L, anti-UV radiation resistance-associated gene (UVRAG), or Rubicon antibodies suggested the formation of ATG14L complex I and UVRAG complex II in G0-podocytes and the formation of Rubicon complex III in G1- and G2-podocytes. These findings suggest that the APOL1 risk alleles favor podocyte dedifferentiation through blockade of multiple autophagy pathways.
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