ArticleCardiovascular drugs and therapy2022
CHOP Increases TRIB3-Dependent miR-208 Expression to Potentiate Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating TIMP3 in Atherosclerosis.
Article in Cardiovascular drugs and therapy, 2022. 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, 16 citations in OpenAlex.
- Predictive value of TRIB3 combined with BMPR2 for major adverse cardiovascular events in elderly coronary heart disease patients undergoing percutaneous coronary intervention.Journal of medical biochemistry · 2026Article
- Role of vascular smooth muscle phenotypic transformation induced by histone modifications in the development of abdominal aortic aneurysms.Clinical epigenetics · 2025Review
- Endoplasmic reticulum-associated degradation mitigates atherosclerosis by maintaining cellular homeostasis.Frontiers in physiology · 2025Review
- Tribbles pseudokinase 3 promoted renal fibrosis by regulating the expression of DNA damage-inducible transcript 3 in diabetic nephropathy.Biomolecules & biomedicine · 2024Article
- C/EBP Homologous Protein: A Potential Therapeutic Target for Atherosclerosis Treatment?Cardiovascular drugs and therapy · 2024Article
- Functional polymorphism in miR-208 is associated with increased risk for ischemic stroke.BMC medical genomics · 2023Article
- Xbp1s-Ddit3 promotes MCT-induced pulmonary hypertension.Clinical science (London, England : 1979) · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundC/EBP homologous protein (CHOP) has been identified as a suitable therapeutic target to combat atherosclerosis but the mechanism has not been fully studied. Here, we sought to define the role and underlying mechanism of CHOP in atherosclerosis.
methodsMouse models of atherosclerosis in ApoE
resultsmiR-208 expression was elevated in atherosclerosis samples and miR-208 overexpression promoted proliferation and migration of VSMCs but diminished plaque stability in mice. TIMP3 was targeted by miR-208, which could be abrogated by upregulation of TIMP3. In addition, CHOP increased TRIB3 expression to upregulate miR-208 and to downregulate TIMP3, which potentiated VSMC proliferation and migration in vitro and in vivo.
conclusionTaken together, inhibition of CHOP may inhibit the proliferation and migration of VSMCs as well as reduce the levels of TC, TG, and LDL-C but increase the level of HDL-C through the TRIB3/miR-208/TIMP3 axis, thereby inhibiting the progression of atherosclerosis.
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