Evidence map›Paper›PMID 40289806›Full record

ArticleCirculation2025

Suppression of the Prostaglandin I2-Type 1 Interferon Axis Induces Extramedullary Hematopoiesis to Promote Cardiac Repair After Myocardial Infarction.

Huizhen Lv, Chenchen Wang, Zening Liu, Meixi Quan, Kan Li, Fanglin Gou, Xuelian Shi, Qian Liu, Ying Yu, Ping Zhu and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Circulation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
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  5. [The blood ecosystem: from concept to practice].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026
    Article
  6. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Huizhen Lv *State Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China.
Chenchen Wang *State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China (C.W., F.G., P.Z., H.C., T.C.).
Zening Liu *State Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China.
Meixi QuanState Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China.
Kan LiState Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China.
Fanglin GouState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China (C.W., F.G., P.Z., H.C., T.C.).
Xuelian ShiState Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China.
Qian LiuSchool of Biomedical Engineering and Technology (Q.L.), Tianjin Medical University, China.ORCID 0000-0002-2788-6222
Ying YuDepartment of Pharmacology, School of Basic Medical Sciences (Y.Y.), Tianjin Medical University, China.ORCID 0000-0002-6476-1752
Ping ZhuState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China (C.W., F.G., P.Z., H.C., T.C.).ORCID 0000-0002-4521-7524
Hui Cheng *State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China (C.W., F.G., P.Z., H.C., T.C.).ORCID 0000-0002-1988-6572
Tao Cheng *State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China (C.W., F.G., P.Z., H.C., T.C.).
Ding Ai *State Key Laboratory of Experimental Hematology, Tianjin Institute of Cardiology, Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Second Hospital of Tianjin Medical University, and Department of Physiology and Pathophysiology (H.L., Z.L., M.Q., K.L., X.S., D.A.), Tianjin Medical University, China.ORCID 0000-0001-5992-9904

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmune cells are closely associated with all processes of cardiac repair after myocardial infarction (MI), including the initiation, development, and resolution of inflammation. Spleen extramedullary hematopoiesis (EMH) serves as a crucial source of emergency mature blood cells that are generated through the self-renewal and differentiation of hematopoietic stem/progenitor cells (HSPCs). However, how EMH responds to MI and the role of EMH in cardiac repair after MI remains unclear.

methodsTo assess the role of spleen EMH in MI, a

resultsWe found that MI enhanced EMH, as reflected by the increase in spleen weight and volume and the number of HSPCs in the spleen. The lack of EMH in

conclusionsTogether, our findings revealed that a PGI2-IFN axis was involved in spleen EMH after MI, providing new mechanistic insights into spleen EMH after MI and offering a new therapeutic target for treating ischemic cardiac injury.

Indexed as

EpoprostenolHematopoiesis, ExtramedullaryInterferon Type IMyocardial InfarctionAnimalsDisease Models, AnimalHematopoietic Stem CellsMaleMiceMice, Inbred C57BLSignal TransductionSpleenEpoprostenolInterferon Type Iextramedullary hematopoiesishematopoietic stem cellsinterferonsmyocardial infarctionprostaglandin

Identifiers

PMID40289806

What OpenQuestion holds

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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.