ArticleJournal of cellular and molecular medicine2024
Endothelial KDM5B Regulated by Piezo1 Contributes to Disturbed Flow Induced Atherosclerotic Plaque Formation.
Article in Journal of cellular and molecular medicine, 2024. 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.
- Review
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Trained Immunity-Like Memory in Vascular Structural Cells: Metabolic-Epigenetic Reprogramming as a Driving Mechanism of Atherosclerosis and Residual Cardiovascular Risk.Journal of inflammation research · 2026Review
- The Mechanosensation-Metabolism-Inflammation Axis: The Central Role of Piezo1 and TRPV4 in Hypertension-Related Atherosclerosis.International journal of general medicine · 2026Review
- AP-1 Is an Initial Convergent Transcriptional Response in Lymphatic Endothelium to VEGF-C or TNFα.Microcirculation (New York, N.Y. : 1994) · 2025Article
- Fumarate Signaling in Cardiovascular Disease: Therapeutic Potential and Pathologic Pitfalls of DMF/MMF and FH1 Deficiency.Journal of cardiovascular translational research · 2025Review
- Role of histone post-translational modifications in atherosclerosis and the therapeutic potential of targeting epigenetic modifiers.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
Epigenetic modifications play an important role in disturbed flow (d-flow) induced atherosclerotic plaque formation. By analysing a scRNA-seq dataset of the left carotid artery (LCA) under d-flow conditions, we found that Jarid1b (KDM5B) was upregulated primarily in a subcluster of endothelial cells in response to d-flow stimulation. We therefore investigated the mechanism of KDM5B expression and the role of KDM5B in endothelial cell. Intriguingly, activation of Piezo1, a major endothelial mechanosensor, was found to promote KDM5B expression, which was reversed by Piezo1 inhibition in HUVECs. Downstream of Piezo1, ETS1 expression and c-JUN phosphorylation were enhanced by d-flow or Piezo1 activation, leading to an increase in KDM5B expression. Furthermore, knockdown of either KDM5B or Piezo1 was found to prevent d-flow induced H3K4me3 demethylation, which was supported by the pharmacological inhibition of Piezo1 in HUVECs. RNA sequencing on shKdm5b HUVECs implied that KDM5B is associated with endothelial inflammation and atherosclerosis. Using partial carotid ligation surgery on Kdm5b
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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 Socratic graph.