Evidence map›Paper›PMID 38952543›Full record

ReviewFrontiers in cardiovascular medicine2024

Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis.

M T La Chica Lhoëst, A Martinez, L Claudi, E Garcia, A Benitez-Amaro, A Polishchuk, J Piñero, D Vilades, J M Guerra, F Sanz and 3 more

Erratum issuedAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Sjogren's Disease and Elevated Cardiovascular Risk: Mechanisms and Treatment.Journal of cardiovascular development and disease · 2025
    Review
  9. Article
  10. Article
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  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

M T La Chica LhoëstDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.
A MartinezDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.
L ClaudiDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.
E GarciaDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.
A Benitez-AmaroDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.
A PolishchukDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.
J PiñeroResearch Programme on Biomedical Informatics (GRIB), Department of Experimental and Health Sciences (DCEXS), Hospital del Mar Medical Research Institute (IMIM), Universitat Pompeu Fabra (UPF), Barcelona, Spain.
D ViladesDepartment of Cardiology, Hospital de la Santa Creu I Sant Pau, Biomedical Research Institute Sant Pau (IIB-SANTPAU), Universitat Autonoma de Barcelona, Barcelona, Spain.
J M GuerraDepartment of Cardiology, Hospital de la Santa Creu I Sant Pau, Biomedical Research Institute Sant Pau (IIB-SANTPAU), Universitat Autonoma de Barcelona, Barcelona, Spain.
F SanzResearch Programme on Biomedical Informatics (GRIB), Department of Experimental and Health Sciences (DCEXS), Hospital del Mar Medical Research Institute (IMIM), Universitat Pompeu Fabra (UPF), Barcelona, Spain.
N RotllanDepartment of Cardiovascular, Institut de Recerca Sant Pau (IR SANT PAU), Barcelona, Spain.
J C Escolà-GilDepartment of Cardiovascular, Institut de Recerca Sant Pau (IR SANT PAU), Barcelona, Spain.
V Llorente-CortésDepartment of Experimental Pathology, Institute of Biomedical Research of Barcelona (IIBB)-Spanish National Research Council (CSIC), Barcelona, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. However, it has been long recognized that diffuse intimal thickening (DIM), which precedes the formation of early fatty streaks in humans, primarily consists of lipid-loaded smooth muscle cells (SMCs) and their secreted proteoglycans. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques. Given that SMCs are a major component of the vascular wall, they serve as a significant source of microvesicles and exosomes, which have the potential to regulate the physiology of other vascular cells. Notably, more than half of the foam cells present in atherosclerotic lesions are of SMC origin. In this review, we describe several mechanisms underlying the formation of intimal foam-like cells in atherosclerotic plaques. Based on these mechanisms, we discuss novel therapeutic approaches that have been developed to regulate the generation of intimal foam-like cells. These innovative strategies hold promise for improving the management of atherosclerosis in the near future.

Indexed as

apoA1apoC1apoE)apoJapolipoproteins (ApoB100atherosclerosiscardiovascular diseasesfoam-like SMClipoproteinspeptidomimeticsreverse cholesterol transporttranscription factors

Identifiers

PMID38952543
PMCPMC11215187

What OpenQuestion holds

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Registered trials

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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.