ArticleJCI insight2022
JAK inhibitor blocks COVID-19 cytokine-induced JAK/STAT/APOL1 signaling in glomerular cells and podocytopathy in human kidney organoids.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Nanotechnology-mediated podocyte injury repair: mechanistic exploration and therapeutic prospects.Renal failure · 2026Review
- Lessons learned: management of acute kidney injury during COVID-19.Renal failure · 2026Article
- Update on APOL1 and chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Differential regulation of basal and interferon-inducedAmerican journal of physiology. Renal physiology · 2026Article
- APOL1 kidney risk variants and outcomes in children with congenital anomalies of the kidney and urinary tract.Pediatric nephrology (Berlin, Germany) · 2026Article
- Viral Mechanisms and Drug Influences on Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) Pathway in Human Coronaviruses Infection: A Systematic Review.Health science reports · 2026Review
- Renal biopsy findings in psoriasis patients with renal involvement: a descriptive clinicopathologic study.BMC nephrology · 2026Article
- Cytokine-Driven Janus Kinase Signal Transducer and Activator of Transcription Pathway Hyperactivity Predicts Disease Severity in Pediatric FSGS.Kidney360 · 2026Article
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- Modelling APOL1-mediated kidney inflammation and fibrosis using a partially reprogrammed urine-derived SIX2-positive renal progenitor cell line.Stem cell research & therapy · 2025Article
- APOL1 kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.Kidney international · 2025Article
- APOL1 risk variants induce metabolic reprogramming of podocytes in patient-derived kidney organoids.Stem cell reports · 2025Article
- Liquid Biopsy-Multiomics Link Adhesion Pathway Dysregulation to Kidney Injury Severity.Kidney international reports · 2025Article
- Review
- Carrying APOL1 G1 allele is associated with cardiovascular complications during COVID-19 in an admixed population.Human genomics · 2025Article
- Epigenetic associations with kidney disease in individuals of African ancestry with APOL1 high-risk genotypes and HIV.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Genetics in Kidney Diseases.Advances in kidney disease and health · 2025Review
- 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
- Precision medicine for focal segmental glomerulosclerosis.Kidney research and clinical practice · 2024Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
COVID-19 infection causes collapse of glomerular capillaries and loss of podocytes, culminating in a severe kidney disease called COVID-19-associated nephropathy (COVAN). The underlying mechanism of COVAN is unknown. We hypothesized that cytokines induced by COVID-19 trigger expression of pathogenic APOL1 via JAK/STAT signaling, resulting in podocyte loss and COVAN phenotype. Here, based on 9 biopsy-proven COVAN cases, we demonstrated for the first time, to the best of our knowledge, that APOL1 protein was abundantly expressed in podocytes and glomerular endothelial cells (GECs) of COVAN kidneys but not in controls. Moreover, a majority of patients with COVAN carried 2 APOL1 risk alleles. We show that recombinant cytokines induced by SARS-CoV-2 acted synergistically to drive APOL1 expression through the JAK/STAT pathway in primary human podocytes, GECs, and kidney micro-organoids derived from a carrier of 2 APOL1 risk alleles, but expression was blocked by a JAK1/2 inhibitor, baricitinib. We demonstrate that cytokine-induced JAK/STAT/APOL1 signaling reduced the viability of kidney organoid podocytes but was rescued by baricitinib. Together, our results support the conclusion that COVID-19-induced cytokines are sufficient to drive COVAN-associated podocytopathy via JAK/STAT/APOL1 signaling and that JAK inhibitors could block this pathogenic process. These findings suggest JAK inhibitors may have therapeutic benefits for managing cytokine-induced, APOL1-mediated podocytopathy.
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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.