ArticleBasic research in cardiology2021
HIMF deletion ameliorates acute myocardial ischemic injury by promoting macrophage transformation to reparative subtype.
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Article in Basic research in cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Vasohibin 1 acts as a key regulator of arrhythmogenesis in pressure-overload-induced cardiac hypertrophy.Acta pharmacologica Sinica · 2026Article
- Morchella polysaccharide ameliorates myocardial infarction inflammation in mice through increasing gut microbiota-derived 12-HEPE.Acta pharmacologica Sinica · 2026Article
- Macrophage PRMT9 Ameliorates Acute Myocardial Infarction by Promoting Symmetric Dimethylation and Degradation of STAT1.Circulation · 2026Article
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- KW-2449 Ameliorates Cardiac Dysfunction in a Rat Model of Sepsis-Induced Cardiomyopathy.Inflammation · 2025Article
- M2 macrophage-derived mitochondrial transplantation promotes periodontal bone regeneration by regulating metabolic homeostasis via activating p38-MAPK signaling pathway.Stem cell research & therapy · 2025Article
- TIMD4JACC. Basic to translational science · 2025Article
- Role of Monocyte/Macrophage-Associated Gene Ccl9 in Acute Myocardial Infarction Analysis: Based on Bulk and Single Cell RNA Sequencing Data.Journal of inflammation research · 2025Article
- Macrophage polarization in acute myocardial infarction: multidimensional regulation and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- IL-4-Induced Gene 1: A Potential Player in Myocardial Infarction.Reviews in cardiovascular medicine · 2024Review
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- Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
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- Potential diagnostic biomarkers: 6 cuproptosis- and ferroptosis-related genes linking immune infiltration in acute myocardial infarction.Genes and immunity · 2023Article
- Article
- Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention.Frontiers in pharmacology · 2023Review
- Adenosine kinase promotes post-infarction cardiac repair by epigenetically maintaining reparative macrophage phenotype.Journal of molecular and cellular cardiology · 2023Article
- TGF-β promotes pericyte-myofibroblast transition in subretinal fibrosis through the Smad2/3 and Akt/mTOR pathways.Experimental & molecular medicine · 2022Article
- Environmental eustress improves postinfarction cardiac repair via enhancing cardiac macrophage survival.Science advances · 2022Article
- Exosomes derived from reparative M2-like macrophages prevent bone loss in murine periodontitis models via IL-10 mRNA.Journal of nanobiotechnology · 2022Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Yanjiao Li *Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Min Dong *Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Qing WangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Santosh KumarGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Rui ZhangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Wanwen ChengGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Jiaqing XiangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Gang WangGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Kunfu OuyangDrug Discovery Center, State Key Laboratory of Chemical Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Peking University, Shenzhen, 51055, China.
Ruxing ZhouGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Yaohong XieGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Yishen LuGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Jing YiGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Haixia DuanGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China.
Jie LiuGuangdong Key Laboratory of Genome Stability and Human Disease Prevention, Department of Pathophysiology, Shenzhen University Health Science Center, Shenzhen, 518060, China. liuj@szu.edu.cn.ORCID http://orcid.org/0000-0001-5310-7520
Shenzhen University Health Science Center · CNPeking University · CNShenzhen University · CN
Funding
Basic Research Foundation of Shenzhen (CN) JCYJ20160308091147262Basic Research Foundation of Shenzhen (CN) JCYJ20170817101514030Basic Research Foundation of Shenzhen (CN) JCYJ20190808121819024Basic Research Foundation of Shenzhen (CN) JCYJ20190808123018993National Natural Science Foundation of China 31671179National Natural Science Foundation of China 81670211National Natural Science Foundation of China 81970250Natural Science Foundation of Guangdong Province (CN) 2018A030310456
Abstract
Appropriately manipulating macrophage M1/M2 phenotypic transition is a promising therapeutic strategy for tissue repair after myocardial infarction (MI). Here we showed that gene ablation of hypoxia-induced mitogenic factor (HIMF) in mice (Himf
Indexed as
RegenerationAnimalsCytokinesDisease Models, AnimalFibroblastsGene DeletionInflammation MediatorsIntercellular Signaling Peptides and ProteinsMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardiumPhenotypeCytokinesDdit3 protein, mouseInflammation MediatorsIntercellular Signaling Peptides and ProteinsRetnla protein, mouseStat1 protein, mouseSTAT1 Transcription FactorStat3 protein, mouseSTAT3 Transcription FactorTranscription Factor CHOPCardiac fibroblastC/EBP-homologous proteinHypoxia-induced mitogenic factorMacrophage polarizationMyocardial infarctionTissue repair
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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.