Evidence map›Paper›PMID 34495326›Full record

ReviewBiochemical Society transactions2021

Mechanisms of vascular smooth muscle cell investment and phenotypic diversification in vascular diseases.

Matthew D Worssam, Helle F Jørgensen

Open access · hybridAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Review
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  7. [Role of the TGFZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
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  12. Review
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  15. Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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

2 authors at 1 institution in 2 countries.

Matthew D WorssamCardiovascular Medicine Division, University of Cambridge, Cambridge, U.K.
Helle F JørgensenCardiovascular Medicine Division, University of Cambridge, Cambridge, U.K.ORCID 0000-0002-7909-2977
University of Cambridge · GB

Funding

British Heart Foundation CH/2000003/12800British Heart Foundation PG/16/11/32021British Heart Foundation PG/16/24/32090British Heart Foundation RG/08/009/25841British Heart Foundation RG/13/14/30314British Heart Foundation RG/20/2/34763
6 · The paper itself

Abstract

In contrast with the heart, the adult mammalian vasculature retains significant remodelling capacity, dysregulation of which is implicated in disease development. In particular, vascular smooth muscle cells (VSMCs) play major roles in the pathological vascular remodelling characteristic of atherosclerosis, restenosis, aneurysm and pulmonary arterial hypertension. Clonal lineage tracing revealed that the VSMC-contribution to disease results from the hyperproliferation of few pre-existing medial cells and suggested that VSMC-derived cells from the same clone can adopt diverse phenotypes. Studies harnessing the powerful combination of lineage tracing and single-cell transcriptomics have delineated the substantial diversity of VSMC-derived cells in vascular lesions, which are proposed to have both beneficial and detrimental effects on disease severity. Computational analyses further suggest that the pathway from contractile VSMCs in healthy arteries to phenotypically distinct lesional cells consists of multiple, potentially regulatable, steps. A better understanding of how individual steps are controlled could reveal effective therapeutic strategies to minimise VSMC functions that drive pathology whilst maintaining or enhancing their beneficial roles. Here we review current knowledge of VSMC plasticity and highlight important questions that should be addressed to understand how specific stages of VSMC investment and phenotypic diversification are controlled. Implications for developing therapeutic strategies in pathological vascular remodelling are discussed and we explore how cutting-edge approaches could be used to elucidate the molecular mechanisms underlying VSMC regulation.

Indexed as

PhenotypeAnimalsAtherosclerosisCell LineageCell PlasticityCell ProliferationGene ExpressionGene Expression RegulationHumansMuscle, Smooth, VascularMyocytes, Smooth MuscleSignal Transductioncardiovascular diseasecell plasticitylineage tracingsingle cell RNA sequencingvascular smooth muscle

Identifiers

PMID34495326
PMCPMC8589433
OpenAlexW3198524042

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.