ArticleKidney international2013
Upregulation of c-mip is closely related to podocyte dysfunction in membranous nephropathy.
Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- "Idiopathic" minimal change nephrotic syndrome: a podocyte mystery nears the end.American journal of physiology. Renal physiology · 2023Review
- Negative intracellular regulators of T-cell receptor (TCR) signaling as potential antitumor immunotherapy targets.Journal for immunotherapy of cancer · 2023Review
- State of the art in childhood nephrotic syndrome: concrete discoveries and unmet needs.Frontiers in immunology · 2023Review
- Review
- The Enigmatic Emerging Role of the C-Maf Inducing Protein in Cancer.Diagnostics (Basel, Switzerland) · 2021Review
- CMIP SNPs and their haplotypes are associated with dyslipidaemia and clinicopathologic features of IgA nephropathy.Bioscience reports · 2020Article
- CMIP is a negative regulator of T cell signaling.Cellular & molecular immunology · 2020Article
- Podocyte Injury in Lupus Nephritis.Journal of clinical medicine · 2019Review
- Minimal change nephrotic syndrome in patients infected with human immunodeficiency virus: a retrospective study of 8 cases.BMC nephrology · 2018Article
- Expression of CMIP in podocytes is restricted to specific classes of lupus nephritis.PloS one · 2018Article
- Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach.Frontiers in medicine · 2018Review
- The association of theInternational journal of clinical and experimental pathology · 2018Article
- Molecular and Cellular Mechanisms for Proteinuria in Minimal Change Disease.Frontiers in medicine · 2018Review
- CMIP Promotes Proliferation and Metastasis in Human Glioma.BioMed research international · 2017Article
- Podocytes.F1000Research · 2016Review
- Transcriptional factors, Mafs and their biological roles.World journal of diabetes · 2015Review
- Immunopathogenesis of idiopathic nephrotic syndrome with relapse.Seminars in immunopathology · 2014Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Membranous nephropathy is a glomerular disease typified by a nephrotic syndrome without infiltration of inflammatory cells or proliferation of resident cells. Although the cause of the disease is unknown, the primary pathology involves the generation of autoantibodies against antigen targets on the surface of podocytes. The mechanisms of nephrotic proteinuria, which reflect a profound podocyte dysfunction, remain unclear. We previously found a new gene, c-mip (c-maf-inducing protein), that was associated with the pathophysiology of idiopathic nephrotic syndrome. Here we found that c-mip was not detected in the glomeruli of rats with passive-type Heymann nephritis given a single dose of anti-megalin polyclonal antibody, yet immune complexes were readily present, but without triggering of proteinuria. Rats reinjected with anti-megalin develop heavy proteinuria a few days later, concomitant with c-mip overproduction in podocytes. This overexpression was associated with the downregulation of synaptopodin in patients with membranous nephropathy, rats with passive Heymann nephritis, and c-mip transgenic mice, while the abundance of death-associated protein kinase and integrin-linked kinase was increased. Cyclosporine treatment significantly reduced proteinuria in rats with passive Heymann nephritis, concomitant with downregulation of c-mip in podocytes. Thus, c-mip has an active role in the podocyte disorders of membranous nephropathy.
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