ArticleEMBO molecular medicine2012
A transcriptional network underlies susceptibility to kidney disease progression.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
8 citing papers in PubMed, 21 citations in OpenAlex.
- Signaling pathways predisposing to chronic kidney disease progression.JCI insight · 2020Article
- MITF - A controls branching morphogenesis and nephron endowment.PLoS genetics · 2017Article
- Spindle pole cohesion requires glycosylation-mediated localization of NuMA.Scientific reports · 2017Article
- Structural basis of selectivity and neutralizing activity of a TGFα/epiregulin specific antibody.Protein science : a publication of the Protein Society · 2016Article
- ADAM17 substrate release in proximal tubule drives kidney fibrosis.JCI insight · 2016Article
- FHL2 switches MITF from activator to repressor of Erbin expression during cardiac hypertrophy.International journal of cardiology · 2015Article
- EGFR signaling in renal fibrosis.Kidney international supplements · 2014Review
- Role of epidermal growth factor receptor in acute and chronic kidney injury.Kidney international · 2013Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular networks that control the progression of chronic kidney diseases (CKD) are poorly defined. We have recently shown that the susceptibility to development of renal lesions after nephron reduction is controlled by a locus on mouse chromosome 6 and requires epidermal growth factor receptor (EGFR) activation. Here, we identified microphthalmia-associated transcription factor A (MITF-A), a bHLH-Zip transcription factor, as a modifier of CKD progression. Sequence analysis revealed a strain-specific mutation in the 5' UTR that decreases MITF-A protein synthesis in lesion-prone friend virus B NIH (FVB/N) mice. More importantly, we dissected the molecular pathway by which MITF-A modulates CKD progression. MITF-A interacts with histone deacetylases to repress the transcription of TGF-α, a ligand of EGFR, and antagonizes transactivation by its related partner, transcription factor E3 (TFE3). Consistent with the key role of this network in CKD, Tgfa gene inactivation protected FVB/N mice from renal deterioration after nephron reduction. These data are relevant to human CKD, as we found that the TFE3/MITF-A ratio was increased in patients with damaged kidneys. Our study uncovers a novel transcriptional network and unveils novel potential prognostic and therapeutic targets for preventing human CKD progression.
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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.