ArticleJournal of molecular and cellular cardiology2015
De-novo collateral formation following acute myocardial infarction: Dependence on CCR2⁺ bone marrow cells.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
- Organ-Specific Efficacy of Postischemic Empagliflozin in Acute Stroke and Myocardial Infarction Using Preclinical Models.Journal of the American Heart Association · 2026Article
- Genetic determinants of insufficiency of the collateral circulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Alternative splicing of the Snap23 microexon is regulated by MBNL, QKI, and RBFOX2 in a tissue-specific manner and is altered in striated muscle diseases.RNA biology · 2025Article
- Plasma microRNA-210 is associated with VEGF-A and EphrinA3 and relates to coronary collateral circulation in patients with coronary heart disease: a cross-sectional study.BMC cardiovascular disorders · 2025Article
- Associations of angiopoietin-like protein 7 with coronary collateral circulation and prognosis of patients with severe coronary artery stenosis.Frontiers in cardiovascular medicine · 2025Article
- Article
- Large differences in collateral blood vessel abundance among individuals arise from multiple genetic variants.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- The Roles of Bone Marrow-Derived Stem Cells in Coronary Collateral Growth Induced by Repetitive Ischemia.Cells · 2023Article
- Impaired post-stroke collateral circulation in sickle cell anemia mice.Frontiers in neurology · 2023Article
- Computational insights on coronary artery function.Nature cardiovascular research · 2022Article
- Blood flow modeling reveals improved collateral artery performance during the regenerative period in mammalian hearts.Nature cardiovascular research · 2022Article
- The essential role for endothelial cell sprouting in coronary collateral growth.Journal of molecular and cellular cardiology · 2022Article
- Role of CCR2-Positive Macrophages in Pathological Ventricular Remodelling.Biomedicines · 2022Review
- Intermittent hypoxia conditioning as a potential prevention and treatment strategy for ischemic stroke: Current evidence and future directions.Frontiers in neuroscience · 2022Review
- Formation and Maintenance of the Natural Bypass Vessels of the Brain.Frontiers in cardiovascular medicine · 2022Review
- Endothelial β1 Integrin-Mediated Adaptation to Myocardial Ischemia.Thrombosis and haemostasis · 2021Article
- High-altitude rodents have abundant collaterals that protect against tissue injury after cerebral, coronary and peripheral artery occlusion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- New Research Is Shining Light on How Collateral Arteries Form in the Heart: a Future Therapeutic Direction?Current cardiology reports · 2021Review
- Decreased inspired oxygen stimulates de novo formation of coronary collaterals in adult heart.Journal of molecular and cellular cardiology · 2021Article
- Coronary vessel formation in development and disease: mechanisms and insights for therapy.Nature reviews. Cardiology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Wide variation exists in the extent (number and diameter) of native pre-existing collaterals in tissues of different strains of mice, with supportive indirect evidence recently appearing for humans. This variation is a major determinant of the wide variation in severity of tissue injury in occlusive vascular disease. Whether such genetic-dependent variation also exists in the heart is unknown because no model exists for study of mouse coronary collaterals. Also owing to methodological limitations, it is not known if ischemia can induce new coronary collaterals to form ("neo-collaterals") versus remodeling of pre-existing ones. The present study sought to develop a model to study coronary collaterals in mice, determine whether neo-collateral formation occurs, and investigate the responsible mechanisms. Four strains with known rank-ordered differences in collateral extent in brain and skeletal muscle were studied: C57BLKS>C57BL/6>A/J>BALB/c. Unexpectedly, these and 5 additional strains lacked native coronary collaterals. However after ligation, neo-collaterals formed rapidly within 1-to-2 days, reaching their maximum extent in ≤7 days. Rank-order for neo-collateral formation differed from the above: C57BL/6>BALB/c>C57BLKS>A/J. Collateral network conductance, infarct volume(-1), and contractile function followed this same rank-order. Neo-collateral formation and collateral conductance were reduced and infarct volume increased in MCP1(-/-) and CCR2(-/-) mice. Bone-marrow transplant rescued collateral formation in CCR2(-/-) mice. Involvement of fractalkine➔CX3CR1 signaling and endothelial cell proliferation were also identified. This study introduces a model for investigating the coronary collateral circulation in mice, demonstrates that neo-collaterals form rapidly after coronary occlusion, and finds that MCP➔CCR2-mediated recruitment of myeloid cells is required for this process.
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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.