ArticleJournal of molecular and cellular cardiology2010
Chronic AMD3100 antagonism of SDF-1alpha-CXCR4 exacerbates cardiac dysfunction and remodeling after myocardial infarction.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 74 citations in OpenAlex.
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- A Comprehensive Review of Dilated Cardiomyopathy in Pre-clinical Animal Models in Addition to Herbal Treatment Options and Multi-modality Imaging Strategies.Cardiovascular & hematological disorders drug targets · 2023Review
- 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
- Role and implications of the CXCL12/CXCR4/CXCR7 axis in atherosclerosis: still a debate.Annals of medicine · 2021Review
- Chemokines in Myocardial Infarction.Journal of cardiovascular translational research · 2021Review
- [Effect of chronic emotional stress induced by empty bottle stimulation on inflammatory factors in rats with acute myocardial infarction: analysis of the CXCL12/CXCR4 axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Dysregulation of Calcium Handling in Duchenne Muscular Dystrophy-Associated Dilated Cardiomyopathy: Mechanisms and Experimental Therapeutic Strategies.Journal of clinical medicine · 2020Review
- Dynamic and Differential Expression of Duplicated Cxcr4/Cxcl12 Genes Facilitates Antiviral Response in Hexaploid Gibel Carp.Frontiers in immunology · 2020Article
- Stromal cell-derived factor-1α signals via the endothelium to protect the heart against ischaemia-reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- Baicalin promotes apoptosis and inhibits proliferation and migration of hypoxia-induced pulmonary artery smooth muscle cells by up-regulating A2a receptor via the SDF-1/CXCR4 signaling pathway.BMC complementary and alternative medicine · 2018Article
- Extracellular ubiquitin modulates cardiac fibroblast phenotype and function via its interaction with CXCR4.Life sciences · 2018Article
- Cathelicidin Related Antimicrobial Peptide (CRAMP) Enhances Bone Marrow Cell Retention and Attenuates Cardiac Dysfunction in a Mouse Model of Myocardial Infarction.Stem cell reviews and reports · 2018Article
- Modeling Idiopathic Pulmonary Fibrosis in Humanized Severe Combined Immunodeficient Mice.The American journal of pathology · 2018Article
- Stromal Cell-Derived Factor-1BioMed research international · 2018Article
- A Novel CXCR4 antagonist enhances angiogenesis via modifying the ischaemic tissue environment.Journal of cellular and molecular medicine · 2017Article
- Circulating fibrocyte mobilization in negative pressure wound therapy.Journal of cellular and molecular medicine · 2017Article
- CXCR4 expression is associated with time-course permanent and temporary myocardial infarction in rats.Iranian journal of basic medical sciences · 2017Article
- Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research.Molecular and cellular biochemistry · 2017Review
- Increased complements and high-sensitivity C-reactive protein predict heart failure in acute myocardial infarction.Biomedical reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The role of the SDF-1alpha-CXCR4 axis in response to myocardial infarction is unknown. We addressed it using the CXCR4 antagonist, AMD3100, to block SDF-1alpha interaction with CXCR4 after chronic coronary artery ligation. Chronic AMD3100 treatment decreased ejection fraction and fractional shortening in mice 20days after myocardial infarction compared with vehicle-treated mice (echocardiography). Morphometric analysis showed hearts of AMD3100-treated infarcted mice to have expanded scar, to be hypertrophic (confirmed by myocyte cross-section area) and dilated, with increased LV end systolic and end diastolic dimensions, and to have decreased scar collagen content; p-AKT levels were attenuated and this was accompanied by increased apoptosis. Despite increased injury, c-kit(pos) cardiac progenitor cells (CPCs) were increased in the risk region of AMD3100-treated infarcted mice; CPCs were CD34(neg)/CD45(neg) with the majority undergoing symmetric cell division. c-kit(pos)/MHC(pos) CPCs also increased in the risk region of the AMD3100-treated infarcted group. In this group, GSK-3beta signaling was attenuated compared to vehicle-treated, possibly accounting for increased proliferation and increased cardiac committed MHC(pos) CPCs. Increased proliferation following AMD3100 treatment was supported by increased levels of cyclin D1, a consequence of increased prolyl isomerase, Pin1, and decreased cyclin D1 phosphorylation. In summary, pharmacologic antagonism of CXCR4 demonstrates that SDF-1alpha-CXCR4 signaling plays an important role during and after myocardial infarction and that it exerts pleiotropic salubrious effects, protecting the myocardium from apoptotic cell death, facilitating scar formation, restricting CPC proliferation, and directing CPCs toward a cardiac fate.
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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.