Evidence map›Paper›PMID 42599177›Full record

ArticleJournal of Zhejiang University. Science. B2026

IL-15 aggravates cardiac ischemic injury via impairing macrophage efferocytosis and driving inflammation.

Lei Guo, Zhehui Yin, Ning Zhang, Han Chen, Zhuo Wang, Yuxue Huang, Jiniu Huang, Yayu You, Chenyun Zhang, Qinyi Bao and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Zhejiang University. Science. B, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Lei GuoDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Zhehui YinDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Ning ZhangDepartment of Cardiology, Hangzhou First Affiliated People's Hospital, Westlake University School of Medicine, Hangzhou 310003, China.
Han ChenDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Zhuo WangDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Yuxue HuangDepartment of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Jiniu HuangDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Yayu YouDepartment of Cardiology, Hunan Provincial People's Hospital, Changsha 410000, China.
Chenyun ZhangDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Qinyi BaoDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Shuxin LeiDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
Jun JiangDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. xiexj@zju.edu.cn.
Xiaojie XieDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. xiexj@zju.edu.cn.

Funding

the National Natural Science Foundation of China 82270498 and 81570322
6 · The paper itself

Abstract

Acute myocardial infarction (AMI) remains a major global health burden and is characterized by profound cardiac inflammation, apoptotic cell death, and impaired myocardial function. While interleukin-15 (IL-15) has been implicated in immune regulation, its precise role in the pathogenesis of AMI has not been clarified. Therefore, this study sought to delineate the functional role of IL-15 in the progression of AMI, with a particular focus on its influence on macrophage-driven inflammation, efferocytosis, and metabolic reprogramming. IL-15 levels were assessed in AMI patients and murine models. To evaluate the impact of IL-15 on cardiac inflammation, apoptosis, and functional outcomes following AMI,

Indexed as

Interleukin-15MacrophagesMyocardial InfarctionMyocardial IschemiaAnimalsApoptosisDisease Models, AnimalEfferocytosisFemaleHumansInflammationInterleukin-15 Receptor alpha SubunitMaleMiceMice, Inbred C57BLMice, KnockoutInterleukin-15Interleukin-15 Receptor alpha SubunitNF-kappa BInflammatory phenotypeInterleukin-15 (IL-15)Macrophage functionMetabolic reprogrammingMyocardial infarction

Identifiers

PMID42599177
PMCPMC13474201

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.