CBS 2019
CBSMD教育中心
中 文

Acute Coronary Syndrom

Abstract

Recommended Article

High-Sensitivity Troponin and The Application of Risk Stratification Thresholds in Patients with Suspected Acute Coronary Syndrome 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines The prognostic role of mid-range ejection fraction in ST-segment elevation myocardial infarction Outcomes in Patients Treated With Thin-Strut, Very Thin-Strut, or Ultrathin-Strut Drug-Eluting Stents in Small Coronary Vessels: A Prespecified Analysis of the Randomized BIO-RESORT Trial Precisely Tuned Inhibition of HIF Prolyl Hydroxylases Is Key for Cardioprotection After Ischemia Impact of Off-Hours Versus On-Hours Primary Percutaneous Coronary Intervention on Myocardial Damage and Clinical Outcomes in ST-Segment Elevation Myocardial Infarction Complete Versus Culprit-Only Lesion Intervention in Patients With Acute Coronary Syndromes Efficacy and Safety of Stents in ST-Segment Elevation Myocardial Infarction

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.