Evidence map›Paper›PMID 35172605›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2022

Crosstalk Between Macrophages and Vascular Smooth Muscle Cells in Atherosclerotic Plaque Stability.

Arif Yurdagul

Abstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
–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

67 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  19. The Pathophysiology of Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Review
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7 more citing papers are in PubMed but not listed here.

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

1 author.

Arif YurdagulDepartment of Molecular and Cellular Physiology, Louisiana State University Health Sciences, Shreveport.ORCID 0000-0002-7613-6313

Funding

Nutrient Sensing of Apoptotic Cells by Macrophages Resolves Inflammation, Drives Atherosclerosis Regression, and Promotes Features of Plaque InstabilityR01HL180481 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI Arif Yurdagul · 2025 to 2026
$1.3M
Processing of Apoptotic Cell-Derived Cargo by Macrophages Continues Efferocytosis and Drives Atherosclerosis RegressionR00HL145131 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI YURDAGUL, ARIF · 2021 to 2023
$747k
NHLBI NIH HHS R00 HL145131NHLBI NIH HHS R01 HL180481
6 · The paper itself

Abstract

Most acute cardiovascular events are due to plaque rupture, with atheromas containing large necrotic cores and thin fibrous caps being more susceptible to rupture and lesions with small necrotic cores and thick fibrous caps being more protected from rupture. Atherosclerotic plaques are comprised various extracellular matrix proteins, modified lipoprotein particles, and cells of different origins, that is, vascular cells and leukocytes. Although much has been revealed about the mechanisms that lead to plaque instability, several key areas remain incompletely understood. This In-Focus Review highlights processes related to cellular crosstalk and the role of the tissue microenvironment in determining cell function and plaque stability. Recent advances highlight critical underpinnings of atherosclerotic plaque vulnerability, particularly impairments in the ability of macrophages to clear dead cells and phenotypic switching of vascular smooth muscle cells. However, these processes do not occur in isolation, as crosstalk between macrophages and vascular smooth muscle cells and interactions with their surrounding microenvironment play a significant role in determining plaque stability. Understanding these aspects of cellular crosstalk within an atherosclerotic plaque may shed light on how to modify cell behavior and identify novel approaches to transform rupture-prone atheromas into stable lesions.

Indexed as

Plaque, AtheroscleroticHumansLeukocyte CountMacrophagesMuscle, Smooth, VascularMyocytes, Smooth Muscleatherosclerosisextracellular matrixlipoproteinsmacrophagesmuscle cells

Identifiers

PMID35172605
PMCPMC8957544

What OpenQuestion holds

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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.