ArticleOncotarget2016
Pharmacological targeting of BET proteins inhibits renal fibroblast activation and alleviates renal fibrosis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- BET inhibitors in cardiovascular diseases: from atherosclerosis to heart failure.Pharmacological reports : PR · 2026Review
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
- Review
- GABP Promotes Mesangial Cell Proliferation and Renal Fibrosis Through GLI1 in Diabetic Nephropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Harnessing the multi-targeted potential of rehmanniae radix natural products against renal fibrosis: a mechanistic review.Frontiers in pharmacology · 2025Review
- BRD4: an effective target for organ fibrosis.Biomarker research · 2024Review
- Delivery of a BET protein degrader via a CEACAM6-targeted antibody-drug conjugate inhibits tumour growth in pancreatic cancer models.Nature communications · 2024Article
- Natural intestinal metabolite xylitol reduces BRD4 levels to mitigate renal fibrosis.Clinical and translational science · 2024Article
- Histone H1.0 couples cellular mechanical behaviors to chromatin structure.Nature cardiovascular research · 2024Article
- Inhibition of BRD4 Attenuates ER Stress-induced Renal Ischemic-Reperfusion Injury.International journal of biological sciences · 2024Article
- Apabetalone Downregulates Fibrotic, Inflammatory and Calcific Processes in Renal Mesangial Cells and Patients with Renal Impairment.Biomedicines · 2023Article
- The epigenetic regulator BRD4 is required for myofibroblast differentiation of knee fibroblasts.Journal of cellular biochemistry · 2023Article
- Type IV Collagen and SOX9 Are Molecular Targets of BET Inhibition in Experimental Glomerulosclerosis.International journal of molecular sciences · 2022Article
- Inhibition of bromodomain extraterminal histone readers alleviates skin fibrosis in experimental models of scleroderma.JCI insight · 2022Article
- Epigenetic Modulation of Gremlin-1/NOTCH Pathway in Experimental Crescentic Immune-Mediated Glomerulonephritis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Histone Acetylation and Modifiers in Renal Fibrosis.Frontiers in pharmacology · 2022Review
- Epigenetics in kidney diseases.Advances in clinical chemistry · 2021Review
- Pharmacologic Targeting of BET Proteins Attenuates Hyperuricemic Nephropathy in Rats.Frontiers in pharmacology · 2021Article
- Enhancer and super-enhancer dynamics in repair after ischemic acute kidney injury.Nature communications · 2020Article
- I-BET151 suppresses osteoclast formation and inflammatory cytokines secretion by targetting BRD4 in multiple myeloma.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Bromodomain and extra-terminal (BET) protein inhibitors have been shown to effectively inhibit tumorgenesis and ameliorate pulmonary fibrosis by targeting bromodomain proteins that bind acetylated chromatin markers. However, their pharmacological effects in renal fibrosis remain unclear. In this study, we examined the effect of I-BET151, a selective and potent BET inhibitor, on renal fibroblast activation and renal fibrosis. In cultured renal interstitial fibroblasts, exposure of cells to I-BET151, or silencing of bromodoma in-containing protein 4 (Brd4), a key BET protein isoform, significantly reduced their activation as indicated by decreased expression of α-smooth muscle actin, collagen 1 and fibronectin. In a murine model of renal fibrosis induced by unilateral ureteral obstruction (UUO), administration of I-BET151 suppressed the deposition of extracellular matrix proteins, renal fibroblast activation and macrophage infiltration. Mechanistically, I-BET151 treatment abrogated UUO-induced phosphorylation of epidermal growth factor receptor and platelet growth factor receptor-β. It also inhibited the activation of Smad-3, STAT3 and NF-κB pathways, as well as the expression of c-Myc and P53 transcription factors in the kidney. Moreover, BET inhibition resulted in the reduction of renal epithelial cells arrested at the G2/M phase of cell cycle after UUO injury. Finally, injury to the kidney up-regulated Brd4, and I-BET151 treatment abrogated its expression. Brd4 was also highly expressed in human fibrotic kidneys. These data indicate that BET proteins are implicated in the regulation of signaling pathways and transcription factors associated with renal fibrogenesis, and suggest that pharmacological inhibition of BET proteins could be a potential treatment for renal fibrosis.
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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.