ArticleJournal of molecular medicine (Berlin, Germany)2016
Cardiomyocyte-derived CXCL12 is not involved in cardiogenesis but plays a crucial role in myocardial infarction.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting pathological chemokines in CVD: the role of saffron on CCL2 and CXCL8.Molecular biology reports · 2026Review
- GATA4-overexpressing BMSCs-derived exosome regulation of myocardial infarction in mice by key miRNA and apoptosis gene CLU.European journal of medical research · 2026Article
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Left ventricular assist device bioinformatics identify possible hubgenes and regulatory networks involved in the myocardium of patients with left ventricular assist device.Frontiers in cardiovascular medicine · 2022Article
- Resveratrol against Cardiac Fibrosis: Research Progress in Experimental Animal Models.Molecules (Basel, Switzerland) · 2021Review
- Smooth Muscle Specific Ablation of CXCL12 in Mice Downregulates CXCR7 Associated with Defective Coronary Arteries and Cardiac Hypertrophy.International journal of molecular sciences · 2021Article
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- The Role of CXC Chemokines in Cardiovascular Diseases.Frontiers in pharmacology · 2021Review
- Comparative Effect of MSC Secretome to MSC Co-culture on Cardiomyocyte Gene Expression Under Hypoxic ConditionsFrontiers in bioengineering and biotechnology · 2020Article
- Article
- Stromal cell-derived factor-1α signals via the endothelium to protect the heart against ischaemia-reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- Exosomal Expression of CXCR4 Targets Cardioprotective Vesicles to Myocardial Infarction and Improves Outcome after Systemic Administration.International journal of molecular sciences · 2019Article
- Have dipeptidyl peptidase-4 inhibitors ameliorated the vascular complications of type 2 diabetes in large-scale trials? The potential confounding effect of stem-cell chemokines.Cardiovascular diabetology · 2018Review
- CXCL12 in Patients with Chronic Kidney Disease and Healthy Controls: Relationships to Ambulatory 24-Hour Blood Pressure and Echocardiographic Measures.Cardiorenal medicine · 2018Observational
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledThe chemokine CXCL12/SDF-1 is crucial for heart development and affects cardiac repair processes due to its ability to attract leukocytes and stem cells to injured myocardium. However, there is a great controversy whether CXCL12 is beneficial or detrimental after myocardial infarction (MI). The divergence in the reported CXCL12 actions may be due to the cellular source and time of release of the chemokine after MI. This study was designed to evaluate the role of cardiomyocyte-derived CXCL12 for cardiogenesis and heart repair after MI. We generated two rodent models each targeting CXCL12 in only one cardiac cell type: cardiomyocyte-specific CXCL12-overexpressing transgenic (Tg) rats and CXCL12 conditional knockout (cKO) mice. Animals of both models did not show any signs of cardiac abnormalities under baseline conditions. After induction of MI, cKO mice displayed preserved cardiac function and remodeling. Moreover, fibrosis was less pronounced in the hearts of cKO mice after MI. Accordingly, CXCL12 Tg rats revealed impaired cardiac function post-MI accompanied by enhanced fibrosis. Furthermore, we observed decreased numbers of infiltrating Th1 cells in the hearts of cKO mice. Collectively, our findings demonstrate that cardiomyocyte-derived CXCL12 is not involved in cardiac development but has adverse effects on the heart after injury via promotion of inflammation and fibrosis. KEY MESSAGES: • CXCL12 in cardiomyocytes is not involved in cardiac development. • CXCL12 deficiency in cardiomyocytes improves outcome of myocardial infarction. • CXCL12 overexpression in cardiomyocytes worsens outcome of myocardial infarction. • CXCL12 increases fibrosis and invasion of Th1 cells in the heart after infarction.
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Registered trials
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.