Evidence map›Paper›PMID 38816371›Full record

ReviewSignal transduction and targeted therapy2024

Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.

Runkai Chen, Hongrui Zhang, Botao Tang, Yukun Luo, Yufei Yang, Xin Zhong, Sifei Chen, Xinjie Xu, Shengkang Huang, Canzhao Liu

Abstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing 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

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

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. β1 Autoantibodies Stimulate T Cells to Become Cardiotoxic.JACC. Basic to translational science · 2026
    Article
  9. Atherosclerotic Cell Fates: A Single-Cell View of ER Stress.Journal of cardiovascular development and disease · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

160 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

10 authors.

Runkai Chen *Department of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China.
Hongrui Zhang *Department of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China.
Botao Tang *Department of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China.
Yukun Luo *Department of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China.
Yufei YangDepartment of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China.
Xin ZhongDepartment of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China.
Sifei ChenState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China.
Xinjie XuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China. xuxinjiepumc@126.com.
Shengkang HuangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100037, China. huangshengkang@fuwai.com.
Canzhao LiuDepartment of Cardiology, Laboratory of Heart Center, Heart Center, Translational Medicine Research Center, Zhujiang Hospital, Southern Medical University, 253 Industrial Avenue, Guangzhou, 510280, China. liucanzhao@smu.edu.cn.ORCID 0000-0002-9035-5723

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune response holds a pivotal role in cardiovascular disease development. As multifunctional cells of the innate immune system, macrophages play an essential role in initial inflammatory response that occurs following cardiovascular injury, thereby inducing subsequent damage while also facilitating recovery. Meanwhile, the diverse phenotypes and phenotypic alterations of macrophages strongly associate with distinct types and severity of cardiovascular diseases, including coronary heart disease, valvular disease, myocarditis, cardiomyopathy, heart failure, atherosclerosis and aneurysm, which underscores the importance of investigating macrophage regulatory mechanisms within the context of specific diseases. Besides, recent strides in single-cell sequencing technologies have revealed macrophage heterogeneity, cell-cell interactions, and downstream mechanisms of therapeutic targets at a higher resolution, which brings new perspectives into macrophage-mediated mechanisms and potential therapeutic targets in cardiovascular diseases. Remarkably, myocardial fibrosis, a prevalent characteristic in most cardiac diseases, remains a formidable clinical challenge, necessitating a profound investigation into the impact of macrophages on myocardial fibrosis within the context of cardiac diseases. In this review, we systematically summarize the diverse phenotypic and functional plasticity of macrophages in regulatory mechanisms of cardiovascular diseases and unprecedented insights introduced by single-cell sequencing technologies, with a focus on different causes and characteristics of diseases, especially the relationship between inflammation and fibrosis in cardiac diseases (myocardial infarction, pressure overload, myocarditis, dilated cardiomyopathy, diabetic cardiomyopathy and cardiac aging) and the relationship between inflammation and vascular injury in vascular diseases (atherosclerosis and aneurysm). Finally, we also highlight the preclinical/clinical macrophage targeting strategies and translational implications.

Indexed as

Cardiovascular DiseasesMacrophagesAnimalsFibrosisHumansInflammation

Identifiers

PMID38816371
PMCPMC11139930

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.