Evidence map›Paper›PMID 39557830›Full record

ArticleSignal transduction and targeted therapy2024

EphrinB2-mediated CDK5/ISL1 pathway enhances cardiac lymphangiogenesis and alleviates ischemic injury by resolving post-MI inflammation.

Yingnan Bai, Liming Chen, Fanghao Guo, Jinghong Zhang, Jinlin Hu, Xuefei Tao, Qing Lu, Wenyi Li, Xueying Chen, Ting Gong and 10 more

Abstract read
In one paragraph

Article 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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

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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

20 authors.

Yingnan Bai *Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China. bai.yingnan@zs-hospital.sh.cn.
Liming Chen *Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Fanghao Guo *Center for Reproductive Medicine & Fertility Preservation Program, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Jinghong ZhangDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Jinlin HuDepartment of Cardiovascular Surgery, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Xuefei TaoDepartment of Geriatric Cardiology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.
Qing LuDepartment of Radiology, Shanghai Dongfang Hospital, Shanghai Tongji University School of Medicine, Shanghai, China.
Wenyi LiDepartment of Endocrinology, Tongren Hospital, Shanghai JiaoMo Tong University School of Medicine, Shanghai, China.
Xueying ChenDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Ting GongDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Nan QiuDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Yawei JinDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Lifan YangDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China.
Yu LeiDepartment of Physiology and Pathophysiology, Shanghai Key Laboratory of Bioactive Small Molecules, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Chengchao RuanDepartment of Physiology and Pathophysiology, Shanghai Key Laboratory of Bioactive Small Molecules, State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.ORCID 0000-0001-5229-9428
Qing JingCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Innovation Center for Intervention of Chronic Disease and Promotion of Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
John P CookeDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, 6670 Bertner Ave., Houston, TX, USA.
Shijun WangDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China. wang.shijun@zs-hospital.sh.cn.
Yunzeng ZouDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China. zou.yunzeng@zs-hospital.sh.cn.ORCID 0000-0003-1871-5496
Junbo GeDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China. ge.junbo2@zs-hospital.sh.cn.ORCID 0000-0002-9360-7332

Funding

Reversal of Heart Failure: Role of Vascular RecoveryR01HL148338 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, KAIFU, COOKE, JOHN P · 2020 to 2023
$2.8M
Role of S-nitrosylation in TransdifferentiationR01HL133254 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI CHEN, KAIFU, COOKE, JOHN P · 2018 to 2021
$1.6M
National Natural Science Foundation of China (National Science Foundation of China) 81900434National Natural Science Foundation of China (National Science Foundation of China) 82170255National Natural Science Foundation of China (National Science Foundation of China) 82200541National Natural Science Foundation of China (National Science Foundation of China) 82230009National Natural Science Foundation of China (National Science Foundation of China) 82430016NHLBI NIH HHS R01 HL133254NHLBI NIH HHS R01 HL148338
6 · The paper itself

Abstract

EphrinB2 (erythropoietin-producing hepatoma interactor B2) is a key Eph/ephrin family member, promoting angiogenesis, vasculogenesis, and lymphangiogenesis during embryonic development. However, the role of EphrinB2 in cardiac lymphangiogenesis following myocardial infarction (MI) and the potential molecular mechanism remains to be demonstrated. This study revealed that EphrinB2 prevented ischemic heart post-MI from remodeling and dysfunction by activating the cardiac lymphangiogenesis signaling pathway. Deletion of EphrinB2 impaired cardiac lymphangiogenesis and aggravated adverse cardiac remodeling and ventricular dysfunction post-MI. At the same time, overexpression of EphrinB2 stimulated cardiac lymphangiogenesis which facilitated cardiac infiltrating macrophage drainage and reduced inflammation in the ischemic heart. The beneficial effects of EphrinB2 on improving clearance of inflammatory response and cardiac function were abolished in Lyve1 knockout mice. Mechanistically, EphrinB2 accelerated cell cycling and lymphatic endothelial cell proliferation and migration by activating CDK5 and CDK5-dependent ISL1 nuclear translocation. EphrinB2 enhanced the transcriptional activity of ISL1 at the VEGFR3 (FLT4) promoter, and VEGFR3 inhibitor MAZ51 significantly diminished the EphrinB2-mediated lymphangiogenesis and deteriorated the ischemic cardiac function. We uncovered a novel mechanism of EphrinB2-driven cardiac lymphangiogenesis in improving myocardial remodeling and function after MI.

Indexed as

Cyclin-Dependent Kinase 5Ephrin-B2LymphangiogenesisMyocardial InfarctionAnimalsHumansInflammationMiceMice, KnockoutSignal TransductionTranscription FactorsVascular Endothelial Growth Factor Receptor-3Cyclin-Dependent Kinase 5EFNB2 protein, mouseEphrin-B2Transcription FactorsVascular Endothelial Growth Factor Receptor-3

Identifiers

PMID39557830
PMCPMC11574162

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.