ArticleThe Journal of clinical investigation2020
Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Epigallocatechin-3-gallate attenuates oxidative stress and apoptosis in podocytes of focal segmental glomerulosclerosis.Renal failure · 2026Article
- Review
- Retinoic Acid Receptor Responder Protein 1 Promotes Tubular Fibrosis via the KH RNA Binding Domain Containing, Signal Transduction Associated 1/Steroid Receptor Coactivator/p-Signal Transducer and Activator of Transcription 3 Axis.Journal of the American Society of Nephrology : JASN · 2026Article
- Review
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Analysis of high glucose injury using human induced pluripotent stem cell-derived kidney organoids.BMC nephrology · 2026Article
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Impaired glycolysis-derived serine metabolism as a key driver of podocyte injury with senescence.Nature communications · 2025Article
- ST32da, a NovelCells · 2025Article
- Elovl7 sensitizes podocytes to ferroptosis in podocytopathy by elongating polyunsaturated fatty acids.Cell death & disease · 2025Article
- Podocytes in health and disease: from development to regeneration.Human cell · 2025Review
- Xanthohumol exerts protective function on adriamycin-induced podocyte injury.European journal of nutrition · 2025Article
- Engineered 3D Kidney Glomerular Microtissues to Model Podocyte-Centric Diseases for the Validation of New Drug Targets.Advanced healthcare materials · 2025Article
- Article
- Inhibition of LINC00707/miR-223-3p/FKBP5 axis has a protective effect on diabetic kidney disease.Journal of diabetes investigation · 2025Article
- Pericytes and Diabetic Microangiopathies: Tissue Resident Mesenchymal Stem Cells with High Plasticity and Regenerative Capacity.International journal of molecular sciences · 2025Review
- Refining the adriamycin-induced focal segmental glomerulosclerosis mouse model to improve reproducibility and animal welfare.Animal models and experimental medicine · 2025Article
- Targeted plasma proteomics reveals organ damage signatures of AIDS- and noncommunicable disease-related deaths in people with HIV.Nature communications · 2025Article
- MiR-203 improved renal cell injury in diabetic nephropathy by targeting SOCS6/SOCS7 and inhibiting JAK/STAT pathway activation.Scientific reports · 2025Article
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16 authors at 5 institutions in 2 countries.
Funding
Abstract
Using the Nephrotic Syndrome Study Network Consortium data set and other publicly available transcriptomic data sets, we identified retinoic acid receptor responder protein 1 (RARRES1) as a gene whose expression positively correlated with renal function decline in human glomerular disease. The glomerular expression of RARRES1, which is largely restricted to podocytes, increased in focal segmental glomerulosclerosis (FSGS) and diabetic kidney disease (DKD). TNF-α was a potent inducer of RARRES1 expression in cultured podocytes, and transcriptomic analysis showed the enrichment of cell death pathway genes with RARRES1 overexpression. The overexpression of RARRES1 indeed induced podocyte apoptosis in vitro. Notably, this effect was dependent on its cleavage in the extracellular domain, as the mutation of its cleavage site abolished the apoptotic effect. Mechanistically, the soluble RARRES1 was endocytosed and interacted with and inhibited RIO kinase 1 (RIOK1), resulting in p53 activation and podocyte apoptosis. In mice, podocyte-specific overexpression of RARRES1 resulted in marked glomerular injury and albuminuria, while the overexpression of RARRES1 cleavage mutant had no effect. Conversely, podocyte-specific knockdown of Rarres1 in mice ameliorated glomerular injury in the setting of adriamycin-induced nephropathy. Our study demonstrates an important role and the mechanism of RARRES1 in podocyte injury in glomerular disease.
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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.