Evidence map›Paper›PMID 40630429›Full record

ReviewReviews in cardiovascular medicine2025

Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis.

Lingna Zhao, Li Zhao, Deshen Liu, Fangze Huang, Qinbao Peng, Jun Lu, Jiaguo Zhou, Shaoyi Zheng, Xiu Liu

Abstract readReview
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Brassinin Induces HMolecules (Basel, Switzerland) · 2025
    Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Lingna ZhaoDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0002-0264-3005
Li ZhaoDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0009-0008-5556-3739
Deshen LiuDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0003-0661-9886
Fangze HuangDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0003-3767-1177
Qinbao PengDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0001-8760-4453
Jun LuDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0009-0002-2036-3119
Jiaguo ZhouDepartment of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-sen University, 510080 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0003-1218-7565
Shaoyi ZhengDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0001-9335-8017
Xiu LiuDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, China.ORCID https://orcid.org/0000-0001-7818-8312

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

apoptosisatherosclerosisautophagyphenotypic switchingvascular smooth muscle cellvascular smooth muscle cell-derived foam cell

Identifiers

PMID40630429
PMCPMC12230849

What Socratic holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

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.