Evidence map›Paper›PMID 35950200›Full record

ArticleRoyal Society open science2022

Macrophage polarization as a potential therapeutic target for atherosclerosis: a dynamic stochastic modelling study.

Mengchen Liu, Yan Cai, Jichao Pan, Karlheinz Peter, Zhiyong Li

Open access · goldAbstract read
In one paragraph

Article in Royal Society open science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Furong Tongmai Capsule Ameliorates Atherosclerosis in ApoEJournal of cellular and molecular medicine · 2026
    Article
  2. Review
  3. 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

5 authors at 3 institutions in 2 countries.

Mengchen LiuSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, People's Republic of China.
Yan CaiSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, People's Republic of China.
Jichao PanSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, People's Republic of China.
Karlheinz PeterAtherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute, PO Box 6492, St Kilda Road Central, Melbourne, VIC 8008, Australia.
Zhiyong LiSchool of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, People's Republic of China.ORCID 0000-0002-6814-9165
Southeast University · CNBaker Heart and Diabetes Institute · AUQueensland University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We proposed a dynamic stochastic mathematical model to evaluate the role of macrophage polarization in plaque development. The dynamic process of macrophages from proliferation to death was simulated under different lipid microenvironments. The probability of macrophage phenotypic switching was described using a Bernoulli distribution where the stochastic variable was determined by the local lipid level. Moreover, the interactions between macrophages and microenvironmental factors vary with macrophage phenotype. We investigated the distribution of key microenvironmental factors, the dynamics of macrophage polarization and its influence on foam cell formation. M1 macrophages were found to predominate in advanced plaque corresponding to the exacerbated inflammation observed in mice experiments. The imbalance between the deposition of oxidized low-density lipoprotein and phagocytic effects of macrophages governed the formation of foam cells. Furthermore, we simulated targeted therapies by either directly inhibiting the polarization probability to M1 macrophages or indirectly regulating macrophage polarization due to high-density lipoprotein levels. Comparison of simulation results with experimental findings in both therapies indicated that the intervention and regulation of macrophage polarization could influence plaque microenvironment and subsequently induce plaque regression, especially in the early stage. The proposed modelling system can facilitate the evaluation of novel therapies targeting macrophage polarization.

Indexed as

macrophagespolarizationtarget therapy

Identifiers

PMID35950200
PMCPMC9346359
OpenAlexW4289526582

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.