Evidence map›Paper›PMID 39460827›Full record

ReviewMolecular and cellular biochemistry2025

Targeting cardiac fibrosis with Chimeric Antigen Receptor-Engineered Cells.

Qinghang Zhang, Jinjie Dai, Tianbao Liu, Wutian Rao, Dan Li, Zhengying Gu, Lin Huang, Jiayi Wang, Xumin Hou

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Engineering Immune Cell to Counteract Aging and Aging-Associated Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  2. CAR-macrophages: a new chapter in cancer immunotherapy.Acta biochimica et biophysica Sinica · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Harnessing chimeric antigen receptor macrophages against solid tumors.Cancer communications (London, England) · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. 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

9 authors.

Qinghang ZhangSchool of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai, 200093, China.
Jinjie DaiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University of Medicine, Shanghai, 200030, China.
Tianbao LiuDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University of Medicine, Shanghai, 200030, China.
Wutian RaoDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University of Medicine, Shanghai, 200030, China.
Dan LiDepartment of Clinical Laboratory Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Zhengying GuDepartment of Clinical Laboratory Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Lin HuangDepartment of Clinical Laboratory Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Jiayi WangDepartment of Clinical Laboratory Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Xumin HouHospital's Office, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. hxmchest@163.com.

Funding

National Natural Science Foundation of China 82172168,82372202
6 · The paper itself

Abstract

Cardiac fibrosis poses a significant challenge in cardiovascular diseases due to its intricate pathogenesis, and there is currently no standardized and effective treatment approach. The fibrotic process entails the involvement of various cell types and molecular mechanisms, such as fibroblast activation and proliferation, increased collagen synthesis, and extracellular matrix rearrangement. Traditional therapies often fall short in efficacy or carry substantial side effects. However, recent studies have shown that Chimeric Antigen Receptor T (CAR-T) cells can selectively target and eliminate activated cardiac fibroblasts (CFs) in mice, leading to reduced cardiac fibrosis and improved myocardial tissue compliance. This breakthrough presents a new and promising avenue for treating cardiac fibrosis. Currently, CAR-T cell-based therapy for cardiac fibrosis is undergoing animal experimentation, indicating ample scope for enhancement. Future investigations could explore the application of CAR cell therapy in cardiac fibrosis treatment, including the potential of CAR-natural killer (CAR-NK) cells and CAR macrophages (CAR-M), offering novel insights and strategies for combating cardiac fibrosis.

Indexed as

MyocardiumReceptors, Chimeric AntigenAnimalsFibroblastsFibrosisHumansKiller Cells, NaturalMacrophagesMiceReceptors, Chimeric AntigenCardiac fibrosisCAR-MCAR-NKCAR-TECM

Identifiers

What OpenQuestion holds

Textmetadata
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.