ReviewReviews in cardiovascular medicine2025
Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis.
Review in Reviews in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed.
- Lipophagy: A key regulator in oxidative stress and metabolic disorders.Genes & diseases · 2026Review
- Review
- Targeting lipophagy in atherosclerosis: Molecular mechanisms, pathogenesis and therapeutic interventions (Review).Molecular medicine reports · 2026Review
- Research Progress on the Molecular Mechanism of LRP1 and TGFβ-PDGFRβ Signaling Network in Atherosclerosis and Vascular Remodeling.International journal of molecular sciences · 2026Review
- EIF2α-ATF4-CHAC1 Signalling Links ER Stress to Ferroptosis in Human Aortic Smooth Muscle Cells: Mechanistic Insights and Therapeutic Implications.Journal of cellular and molecular medicine · 2026Article
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- The primary cilium-autophagy axis in vascular homeostasis and cardiovascular disease: mechanistic crosstalk and evidence boundaries.Frontiers in cardiovascular medicine · 2026Review
- Prodrug Strategies in Atherosclerosis: Targeted Delivery and Therapeutic Advances.Cardiovascular therapeutics · 2026Review
- Brassinin Induces HMolecules (Basel, Switzerland) · 2025Article
- Tumor-like characteristics of vascular smooth muscle cells in atherosclerosis.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Vascular smooth muscle cells (VSMCs) are involved in atherosclerotic plaque development. The formation of VSMC-originated foam cells, phenotypic switching, and VSMC proliferation, migration, apoptosis, and autophagy play different roles in atherosclerosis (AS). Main Body: Foam cell formation promotes the generation and evolution of atherosclerotic plaques. The VSMC phenotype, switching from contractile to other forms, is important in the formation and progression of AS. VSMC proliferation, migration, and apoptosis affect the stability of atherosclerotic plaques through the fibrous cap. VSMC proliferation and migration can increase the thickness of the fibrous cap of the plaques, which protects plaques from rupture and is beneficial for slowing the occurrence of advanced lesions. However, apoptosis can accelerate plaque rupturing and trigger severe cardiovascular disease. The autophagy of VSMCs has a protective influence on safeguarding cellular homeostasis in the early stages of AS. However, increased autophagy of VSMCs in the late stages of AS can lead to cell death, thereby affecting the stability of late-stage plaques. This review comprehensively reviews recent research on genetic proteins and mechanisms influencing various aspects of VSMCs, including VSMC-derived foam cells, phenotypic switching, proliferation, migration, apoptosis, and autophagy. Additionally, this review aimed to examine the implications of VSMCs for AS and discussed several regulators that can impact the progression of this condition. Our review thoroughly summarizes the latest research developments in this field. Conclusion: Based on the vital role of VSMCs in AS, this review provides an overview of the latest factors and mechanisms based on VSMC-derived foam cells, phenotype switching, proliferation, migration, apoptosis, and autophagy. The review also introduces certain regulators that can inhibit the development of AS. An understanding of the role of VSMCs aids in identifying new targets and directions for advancing innovative anti-atherosclerotic therapeutic regimens and provides new insights into the development of treatments for AS.
Indexed as
Identifiers
What Socratic 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 Socratic graph.