Evidence map›Paper›PMID 39377453›Full record

ArticleCell proliferation2025

Modelling myocardial ischemia/reperfusion injury with inflammatory response in human ventricular cardiac organoids.

Laihai Zhang, Yun Jiang, Wenwen Jia, Wenjun Le, Jie Liu, Peng Zhang, Huangtian Yang, Zhongmin Liu, Yang Liu

Abstract read
In one paragraph

Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Human cardiovascular organoids: Biomedical applications and ethical challenges.American heart journal plus : cardiology research and practice · 2026
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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.

Laihai ZhangShanghai Heart Failure Research Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Yun JiangInstitute for Regenerative Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Wenwen JiaNational Stem Cell Translational Resource Center, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Wenjun LeInstitute for Regenerative Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Jie LiuShanghai Heart Failure Research Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Peng ZhangInstitute for Regenerative Medicine, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Huangtian YangShanghai Heart Failure Research Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0002-6297-9037
Zhongmin LiuShanghai Heart Failure Research Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Yang LiuShanghai Heart Failure Research Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID https://orcid.org/0000-0002-0493-5466

Funding

National Key Research and Development Program of China 2022YFA1104500National Key Research and Development Program of China 2022YFA1105100National Natural Science Foundation of China 82100272National Natural Science Foundation of China 82270260Peak Disciplines (Type IV) of Institutions of Higher Learning in Shanghai
6 · The paper itself

Abstract

Current therapeutic drug exploring targeting at myocardial ischemia/reperfusion (I/R) injury is limited due to the lack of humanized cardiac models that resemble myocardial damage and inflammatory response. Herein, we develop ventricular cardiac organoids from human induced pluripotent stem cells (hiPSCs) and simulate I/R injury by hypoxia/reoxygenation (H/R), which results in increased cardiomyocytes apoptosis, elevated oxidative stress, disrupted morphological structure and decreased beat amplitude. RNA-seq reveals a potential role of type I interferon (IFN-I) in this I/R injury model. We then introduce THP-1 cells and reveal inflammatory responses between monocytes/macrophages and H/R-induced ventricular cardiac organoids. Furthermore, we demonstrate Anifrolumab, an FDA approved antagonist of IFN-I receptor, effectively decreases IFN-I secretion and related gene expression, attenuates H/R-induced inflammation and oxidative stress in the co-culture system. This study advances the modelling of myocardial I/R injury with inflammatory response in human cardiac organoids, which provides a reliable platform for preclinical study and drug screening.

Indexed as

Heart VentriclesInflammationMyocardial Reperfusion InjuryOrganoidsApoptosisCoculture TechniquesHumansInduced Pluripotent Stem CellsInterferon Type IMyocytes, CardiacOxidative StressInterferon Type I

Identifiers

PMID39377453
PMCPMC11882745

What Socratic 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 Socratic graph.