Evidence map›Paper›PMID 38873669›Full record

ReviewHeliyon2024

Macrophage polarisation and inflammatory mechanisms in atherosclerosis: Implications for prevention and treatment.

Bo Yang, Sanhua Hang, Siting Xu, Yun Gao, Wenhua Yu, Guangyao Zang, Lili Zhang, Zhongqun Wang

Abstract readReview
In one paragraph

Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Anti-Atherogenic Mechanisms and Therapies.Current atherosclerosis reports · 2025
    Review
  16. Review
  17. Research progress on macrophages in cardiovascular diseases.Journal of cardiothoracic surgery · 2025
    Review
  18. Article
  19. Article
  20. 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

8 authors.

Bo YangDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Sanhua HangDepartment of Hematology, Affiliated Danyang Hospital of Nantong University, Danyang, 212300, China.
Siting XuDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Yun GaoDepartment of Pathology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Wenhua YuDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Guangyao ZangDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Lili ZhangDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.
Zhongqun WangDepartment of Cardiology, Affiliated Hospital of Jiangsu University, Zhenjiang, 212001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease characterised by plaque accumulation in the arteries. Macrophages are immune cells that are crucial in the development of atherosclerosis. Macrophages can adopt different phenotypes, with the M1 phenotype promoting inflammation while the M2 phenotype counteracting it. This review focuses on the factors that drive the polarisation of M1 macrophages towards a pro-inflammatory phenotype during AS. Additionally, we explored metabolic reprogramming mechanisms and cytokines secretion by M1 macrophages. Hyperlipidaemia is widely recognised as a major risk factor for atherosclerosis. Modified lipoproteins released in the presence of hyperlipidaemia can trigger the release of cytokines and recruit circulating monocytes, which adhere to the damaged endothelium and differentiate into macrophages. Macrophages engulf lipids, leading to the formation of foam cells. As atherosclerosis progresses, foam cells become the necrotic core within the atherosclerotic plaques, destabilising them and triggering ischaemic disease. Furthermore, we discuss recent research focusing on targeting macrophages or inflammatory pathways for preventive or therapeutic purposes. These include statins, PCSK9 inhibitors, and promising nanotargeted drugs. These new developments hold the potential for the prevention and treatment of atherosclerosis and its related complications.

Indexed as

AtherosclerosisM1 macrophagesMetabolismNanomedicine

Identifiers

PMID38873669
PMCPMC11170185

What OpenQuestion holds

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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 OpenQuestion graph.