ArticleAmerican journal of translational research2018
BMAL1 suppresses ROS-induced endothelial-to-mesenchymal transition and atherosclerosis plaque progression via BMP signaling.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Histone modification of endothelial-mesenchymal transition in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Pooled it
- Circadian mechanisms in heart failure: Cell-specific regulation and chrono-medicine.Cell insight · 2026Review
- BMAL1 in cardiovascular diseases: Molecular mechanisms, circadian regulation and translational perspectives (Review).Molecular medicine reports · 2026Review
- Circadian-driven transcriptional programs govern metastatic progression.Cancer biology & medicine · 2026Review
- Circadian rhythm and the molecular clock in endothelial function of the cardiovascular system.Molecular and cellular biochemistry · 2026Review
- Comprehensive bioinformatics analysis and experimental validation reveal the role of circadian rhythm-related genes in the crosstalk between osteoporosis and atherosclerosis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Circadian disruption and circulating TGF-β1 in workers: evidence from Mendelian randomization and observational data.Frontiers in immunology · 2026Observational
- Endothelial-to-mesenchymal transition in atherosclerosis: mechanisms, therapeutic targets, and future perspectives.Frontiers in cell and developmental biology · 2026Review
- Association ofInternational journal of molecular sciences · 2025Article
- Achilles tendinopathy treatment via circadian rhythm regulation.Journal of advanced research · 2025Article
- The role of miR-155 in cardiovascular diseases: Potential diagnostic and therapeutic targets.International journal of cardiology. Cardiovascular risk and prevention · 2025Review
- Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review.Bone research · 2025Review
- Elucidating the crosstalk between endothelial-to-mesenchymal transition (EndoMT) and endothelial autophagy in the pathogenesis of atherosclerosis.Vascular pharmacology · 2024Review
- Effect of reactive oxygen, nitrogen, and sulfur species on signaling pathways in atherosclerosis.Vascular pharmacology · 2024Review
- PPARγ (Peroxisome Proliferator-Activated Receptor γ) Deacetylation Suppresses Aging-Associated Atherosclerosis and Hypercholesterolemia.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Low intensity near-infrared light promotes bone regeneration via circadian clock protein cryptochrome 1.International journal of oral science · 2022Article
- Importance of Bmal1 in Alzheimer's disease and associated aging-related diseases: Mechanisms and interventions.Aging cell · 2022Review
- The Role of Circadian Clock Genes in Critical Illness: The Potential Role of Translational Clock Gene Therapies for Targeting Inflammation, Mitochondrial Function, and Muscle Mass in Intensive Care.Journal of biological rhythms · 2022Review
- Mitochondrial dysfunction in vascular endothelial cells and its role in atherosclerosis.Frontiers in physiology · 2022Review
- A wrinkle in time: circadian biology in pulmonary vascular health and disease.American journal of physiology. Lung cellular and molecular physiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circadian rhythm disruption is intimately linked to atherosclerosis, and endothelial-to-mesenchymal transition (EndMT) is a major feature of atherosclerosis progression and unstable plaques. However, the mechanisms underlying the roles of Brain and Muscle ARNT-Like Protein-1 (BMAL1), an essential clock transcription activator, in EndMT and plaque instability have not been characterized. In the present study, we found a positive relationship among BMAL1 expression loss, EndMT, and plaque vulnerability in human carotid plaques. Furthermore, loss- and gain-of-function studies in human aortic endothelial cells (HAECs) revealed that BMAL1 inhibited oxidized low-density lipoprotein (oxLDL)-induced intracellular reactive oxygen species (ROS) accumulation and subsequent EndMT. Mechanistically, BMAL1 deficiency aggravated EndMT through BMP-mediated signaling. Collectively, our study demonstrates the underlying mechanism for the central role of BMAL1 loss in atherosclerosis progression and plaque stability transition promoted by oxidative stress, which can be targeted therapeutically to prevent the occurrence and progression of atherosclerosis.
Indexed as
Identifiers
30416657PMC6220214W2985774746What OpenQuestion holds
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.