ArticleScientific reports2019
Disruption of APOL1-miR193a Axis Induces Disorganization of Podocyte Actin Cytoskeleton.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 28 citations in OpenAlex.
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- APOL1 kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.Kidney international · 2025Article
- APOL1 Dynamics in Diabetic Kidney Disease and Hypertension.Biomolecules · 2025Review
- APOL1 Modulates Renin-Angiotensin System.Biomolecules · 2024Article
- Potential biomarkers of recurrent FSGS: a review.BMC nephrology · 2024Review
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- The metabolic effects of APOL1 in humans.Pflugers Archiv : European journal of physiology · 2023Review
- Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a.Biomolecules · 2023Review
- Inhibition of endoplasmic reticulum stress signaling rescues cytotoxicity of human apolipoprotein-L1 risk variants in Drosophila.Kidney international · 2022Article
- The evolving story of apolipoprotein L1 nephropathy: the end of the beginning.Nature reviews. Nephrology · 2022Review
- APOL1 risk variants and the development of HIV-associated nephropathy.The FEBS journal · 2021Review
- Recessive, gain-of-function toxicity in an APOL1 BAC transgenic mouse model mirrors human APOL1 kidney disease.Disease models & mechanisms · 2021Article
- Article
- APOL1 risk variants affect podocyte lipid homeostasis and energy production in focal segmental glomerulosclerosis.Human molecular genetics · 2021Article
- A focus on the association of Apol1 with kidney disease in children.Pediatric nephrology (Berlin, Germany) · 2021Review
- Lessons From APOL1 Animal Models.Frontiers in medicine · 2021Review
- Gangliosides in Podocyte Biology and Disease.International journal of molecular sciences · 2020Review
- The clinical significance of apolipoprotein L1 in head and neck squamous cell carcinoma.Oncology letters · 2020Article
- Alterations in plasma membrane ion channel structures stimulate NLRP3 inflammasome activation in APOL1 risk milieu.The FEBS journal · 2020Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
APOL1-miR193a axis participates in the preservation of molecular phenotype of differentiated podocytes (DPDs). We examined the hypothesis that APOL1 (G0) preserves, but APOL1 risk alleles (G1 and G2) disrupt APOL1-miR193a axis in DPDs. DPDG0s displayed down-regulation of miR193a, but upregulation of nephrin expression. DPDG1s/G2s exhibited an increase in miR193a and down-regulation of the expression of adherens complex's constituents (CD2AP, nephrin, and dendrin). DPDG0s showed decreased Cathepsin L, enhanced dynamin expressions, and the intact actin cytoskeleton. On the contrary, DPDG1s/G2s displayed an increase in Cathepsin L, but down-regulation of dynamin expressions and disorganization of the actin cytoskeleton. APOL1 silencing enhanced miR193a and Cathepsin L, but down-regulated dynamin expressions. DPDG1s/G2s displayed nuclear import of dendrin, indicating an occurrence of destabilization of adherens complexes in APOL1 risk milieu. These findings suggest that DPDG1s and DPDG2s developed disorganized actin cytoskeleton as a consequence of disrupted APOL1-miR193a axis. Interestingly, docking and co-labeling studies suggested an interaction between APOL1 and CD2AP. APOL1
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.