ArticleThe Journal of clinical investigation2003
JunD protects against chronic kidney disease by regulating paracrine mitogens.
Article in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 57 citations in OpenAlex.
- Scutellarin prevents obesity-induced renal fibrosis via reduced activation of AP-1.Journal of translational medicine · 2025Article
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- Signaling pathways predisposing to chronic kidney disease progression.JCI insight · 2020Article
- Proximal Tubule Translational Profiling during Kidney Fibrosis Reveals Proinflammatory and Long Noncoding RNA Expression Patterns with Sexual Dimorphism.Journal of the American Society of Nephrology : JASN · 2020Article
- Novel Biomarkers in the Diagnosis of Chronic Kidney Disease and the Prediction of Its Outcome.International journal of molecular sciences · 2017Review
- Spindle pole cohesion requires glycosylation-mediated localization of NuMA.Scientific reports · 2017Article
- The JNK Signaling Pathway in Renal Fibrosis.Frontiers in physiology · 2017Review
- Transcriptional regulation of importin-α1 by JunD modulates subcellular localization of RNA-binding protein HuR in intestinal epithelial cells.American journal of physiology. Cell physiology · 2016Article
- Stat3 Controls Tubulointerstitial Communication during CKD.Journal of the American Society of Nephrology : JASN · 2016Article
- Transplant-induced reactivation of murine cytomegalovirus immediate early gene expression is associated with recruitment of NF-κB and AP-1 to the major immediate early promoter.The Journal of general virology · 2016Article
- β-Arrestin scaffolds and signaling elements essential for the obestatin/GPR39 system that determine the myogenic program in human myoblast cells.Cellular and molecular life sciences : CMLS · 2016Article
- Association between renal iron accumulation and renal interstitial fibrosis in a rat model of chronic kidney disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- JunD enhances miR-29b levels transcriptionally and posttranscriptionally to inhibit proliferation of intestinal epithelial cells.American journal of physiology. Cell physiology · 2015Article
- Hypertensive renal injury is associated with gene variation affecting immune signaling.Circulation. Cardiovascular genetics · 2014Article
- Role of kidney biomarkers of chronic kidney disease: An update.Saudi journal of biological sciences · 2014Review
- Signal transduction in podocytes--spotlight on receptor tyrosine kinases.Nature reviews. Nephrology · 2014Review
- Increased renal iron accumulation in hypertensive nephropathy of salt-loaded hypertensive rats.PloS one · 2013Article
- A transcriptional network underlies susceptibility to kidney disease progression.EMBO molecular medicine · 2012Article
- A look at transactivation of the EGF receptor by angiotensin II.Journal of the American Society of Nephrology : JASN · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AP-1 transcription factor, composed of Jun and Fos proteins, plays a crucial role in the fine tuning of cell proliferation. We showed previously that AP-1 complexes are activated during the proliferative response that parallels the development of renal lesions after nephron reduction, but little is known about the specific role of individual Jun/Fos components in the deterioration process. Here we used JunD knockout (JunD-/-) mice and an experimental model of chronic renal injury (75% nephron reduction) to explore the role of JunD. Nephron reduction resulted in an initial compensatory growth phase that did not require JunD. JunD, however, was essential to inhibit a second wave of cell proliferation and to halt the development of severe glomerular sclerosis, tubular dilation, and interstitial fibrosis. We show that the effects of junD inactivation are not cell autonomous and involve upregulation of the paracrine mitogen, TGF-alpha. Expression of a transgene (REM) encoding a dominant negative isoform of the EGFR, the receptor for TGF-alpha, prevented the second wave of cell proliferation and the development of renal lesions in bitransgenic JunD-/-/REM mice. We propose that JunD is part of a regulatory network that controls proliferation to prevent pathological progression in chronic renal diseases.
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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.