ArticleFrontiers in microbiology2023
HCMV-IE2 promotes atherosclerosis by inhibiting vascular smooth muscle cells' pyroptosis.
Article in Frontiers in microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- HCMV infection disrupts barrier functions and promotes epithelial-mesenchymal transition in a cholangiocyte organoid model.Nature communications · 2026Article
- Targeting pyroptosis in atherosclerosis: emerging pharmacologic strategies and natural compound-based therapeutics-a narrative review.International journal of clinical pharmacy · 2026Review
- Article
- Molecular mechanisms of HCMV-driven vascular remodeling and its significance in cardiovascular diseases.Archives of microbiology · 2025Review
- A New Insight on Atherosclerosis Mechanism and Lipid-Lowering Drugs.Reviews in cardiovascular medicine · 2025Review
- Advances in molecular regulation and function of LDLR family in viral infection.Frontiers in microbiology · 2025Review
- Human cytomegalovirus-IE2 suppresses antigen presentation of macrophage through the IL10/STAT3 signalling pathway in transgenic mouse.PloS one · 2025Article
- The serum levels of gasdermin D in uremic patients and its relationship with the prognosis: a prospective observational cohort study.Renal failure · 2024Observational
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is still the main cause of death in developed and developing countries. Vascular smooth muscle cells (VSMCs) death disorder is a key pathogens of atherosclerosis. During the early stage of human cytomegalovirus (HCMV) infection, immediate early protein 2 (IE2) is critical in regulating its host cell death to ensure HCMV replication. Abnormal cell death induced by HCMV infection contributes to the development of numerous diseases, including atherosclerosis. Hitherto, the underlying mechanism of HCMV involved in the progression of atherosclerosis is still unclear. In this study, the infection models
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