ArticleThe American journal of pathology2004
Inhibition of p38 mitogen-activated protein kinase augments progression of remnant kidney model by activating the ERK pathway.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 38 citations in OpenAlex.
- ASK1 contributes to fibrosis and dysfunction in models of kidney disease.The Journal of clinical investigation · 2018Article
- Article
- Effects of the mTOR inhibitor rapamycin on monocyte-secreted chemokines.BMC immunology · 2014Article
- Phosphorylation of DGCR8 increases its intracellular stability and induces a progrowth miRNA profile.Cell reports · 2013Article
- Inhibition of p38 MAPK attenuates renal atrophy and fibrosis in a murine renal artery stenosis model.American journal of physiology. Renal physiology · 2013Article
- Article
- Inhibition of p38 mitogen-activated protein kinase and transforming growth factor-beta1/Smad signaling pathways modulates the development of fibrosis in adriamycin-induced nephropathy.The American journal of pathology · 2006Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
p38, a mitogen-activated protein kinase, is a major intracellular signaling molecule involved in inflammation. To test the hypothesis that p38 mediates renal disease progression, we administered a novel p38 alpha inhibitor, NPC31169, to rats with remnant kidneys (RKs). RK rats showed increased p38 activation at 9 weeks (by p38 kinase assay), which was blocked by the inhibitor. In contrast to our expectation, treatment with the NPC31169 resulted in worse renal function, more proteinuria, and more severe glomerulosclerosis and tubulointerstitial injury. p38 inhibition resulted in marked cell proliferation in RK rats, with more proliferating tubular cells, myofibroblasts, and macrophages. In contrast, p38 suppression resulted in less tubular cell apoptosis. Interestingly, Western blot demonstrated increased ERK1/2 phosphorylation in p38-treated rats. No histological changes were observed in p38 inhibited sham-operated rats. Our findings indicate that, whereas blocking p38 usually shows benefit in inflammatory disease, in this model p38 inhibition resulted in accelerated renal progression. We conclude that blocking p38-dependent inflammation may have resulted in enhanced proliferation and increased ERK1/2 activation, and thereby explains the worse renal lesions observed.
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