Evidence map›Paper›PMID 39133247›Full record

ReviewCurrent atherosclerosis reports2024

Targeting Macrophage Phenotypes and Metabolism as Novel Therapeutic Approaches in Atherosclerosis and Related Cardiovascular Diseases.

Juan Wang, Qiang Wu, Xinyu Wang, Hongbin Liu, Mulei Chen, Li Xu, Ze Zhang, Kuibao Li, Weiming Li, Jiuchang Zhong

Abstract readReview
In one paragraph

Review in Current atherosclerosis reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Macrophages on demand: How tissue trauma shapes their role.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  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

10 authors.

Juan WangBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China. wangjuan.goal@163.com.
Qiang WuSenior Department of Cardiology, the Sixth Medical Center, Chinese PLA General Hospital, Beijing, China.
Xinyu WangBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Hongbin LiuDepartment of Cardiology, the Second Medical Center, National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China.
Mulei ChenBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Li XuBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Ze ZhangNational Institute of Biological Sciences, Beijing, China.
Kuibao LiBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Weiming LiBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China. liweiming@sina.com.
Jiuchang ZhongBeijing Key Laboratory of Hypertension, Heart Center of Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China. jczhong@sina.com.

Funding

JC.Z. Beijing Municipal Natural Science Foundation 7222068JC.Z. National Natural Science Fund 92168117J.W. Beijing Municipal Natural Science Foundation, 7222072 7222072J.W. National Natural Science Fund 81900382
6 · The paper itself

Abstract

purpose of the reviewMacrophage accumulation and activation function as hallmarks of atherosclerosis and have complex and intricate dynamics throughout all components and stages of atherosclerotic plaques. In this review, we focus on the regulatory roles and underlying mechanisms of macrophage phenotypes and metabolism in atherosclerosis. We highlight the diverse range of macrophage phenotypes present in atherosclerosis and their potential roles in progression and regression of atherosclerotic plaque. Furthermore, we discuss the challenges and opportunities in developing therapeutic strategies for preventing and treating atherosclerotic cardiovascular disease. RECENT

findingsDysregulation of macrophage polarization between the proinflammatory M1 and anti-inflammatory M2 phenotypealters the immuno-inflammatory response during atherosclerosis progression, leading to plaque initiation, growth, and ultimately rupture. Altered metabolism of macrophage is a key feature for their function and the subsequent progression of atherosclerotic cardiovascular disease. The immunometabolism of macrophage has been implicated to macrophage activation and metabolic rewiring of macrophages within atherosclerotic lesions, thereby shifting altered macrophage immune-effector and tissue-reparative function. Targeting macrophage phenotypes and metabolism are potential therapeutic strategies in the prevention and treatment of atherosclerosis and atherosclerotic cardiovascular diseases. Understanding the precise function and metabolism of specific macrophage subsets and their contributions to the composition and growth of atherosclerotic plaques could reveal novel strategies to delay or halt development of atherosclerotic cardiovascular diseases and their associated pathophysiological consequences. Identifying biological stimuli capable of modulating macrophage phenotypes and metabolism may lead to the development of innovative therapeutic approaches for treating patients with atherosclerosis and coronary artery diseases.

Indexed as

AtherosclerosisMacrophagesPhenotypeAnimalsCardiovascular DiseasesHumansMacrophage ActivationPlaque, AtheroscleroticAtherosclerosisCoronary artery diseasesMacrophageMetabolismPhenotype

Identifiers

PMID39133247
PMCPMC11392985

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.