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急性冠脉综合征

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MR-proADM as a Prognostic Marker in Patients With ST-Segment-Elevation Myocardial Infarction-DANAMI-3 (a Danish Study of Optimal Acute Treatment of Patients With STEMI) Substudy Prevalence of anginal symptoms and myocardial ischemia and their effect on clinical outcomes in outpatients with stable coronary artery disease: data from the International Observational CLARIFY Registry Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction Late Survival Benefit of Percutaneous Coronary Intervention Compared With Medical Therapy in Patients With Coronary Chronic Total Occlusion: A 10-Year Follow-Up Study Association Between Collateral Circulation and Myocardial Viability Evaluated by Cardiac Magnetic Resonance Imaging in Patients With Coronary Artery Chronic Total Occlusion 4-Step Protocol for Disparities in STEMI Care and Outcomes in Women Heart Regeneration by Endogenous Stem Cells and Cardiomyocyte Proliferation: Controversy, Fallacy, and Progress Myocardial infarction with non-obstructive coronary arteries as compared with myocardial infarction and obstructive coronary disease: outcomes in a Medicare population Early versus delayed invasive intervention in acute coronary syndromes Colchicine Inhibits Neutrophil Extracellular Trap Formation in Patients With Acute Coronary Syndrome After Percutaneous Coronary Intervention

Original Researcholume 74, Issue 25, December 2019

JOURNAL:J Am Coll Cardiol. Article Link

Transition of Macrophages to Fibroblast-Like Cells in Healing Myocardial Infarction

N Haider, L Boscá, HR Zandbergen et al. Keywords: cardiac fibroblast; fibroblast markers; infiltration; macrophage/fibroblast-like transition; myeloid tracers; MI

ABSTRACT


BACKGROUND - Macrophages and fibroblasts are 2 major cell types involved in healing after myocardial infarction (MI), contributing to myocardial remodeling and fibrosis. Post-MI fibrosis progression is characterized by a decrease in cardiac macrophage content.


OBJECTIVES - This study explores the potential of macrophages to express fibroblast genes and the direct role of these cells in post-MI cardiac fibrosis.


METHODS - Prolonged in vitro culture of human macrophages was used to evaluate the capacity to express fibroblast markers. Infiltrating cardiac macrophages was tracked in vivo after experimental MI of LysM(Cre/+);ROSA26(EYFP/+) transgenic mice. The expression of Yellow Fluorescent Protein (YFP) in these animals is restricted to myeloid lineage allowing the identification of macrophage-derived fibroblasts. The expression in YFP-positive cells of fibroblast markers was determined in myocardial tissue sections of hearts from these mice after MI.


RESULTS - Expression of the fibroblast markers type I collagen, prolyl-4-hydroxylase, fibroblast specific protein-1, and fibroblast activation protein was evidenced in YFP-positive cells in the heart after MI. The presence of fibroblasts after MI was evaluated in the hearts of animals after depletion of macrophages with clodronate liposomes. This macrophage depletion significantly reduced the number of Mac3+Col1A1+ cells in the heart after MI.


CONCLUSIONS -  The data provide both in vitro and in vivo evidence for the ability of macrophages to transition and adopt a fibroblast-like phenotype. Therapeutic manipulation of this macrophage-fibroblast transition may hold promise for favorably modulating the fibrotic response after MI and after other cardiovascular pathological processes.