Why the study?
Despite reduced mortality after acute myocardial infarction, it remains the leading cause of heart failure, and highly efficient experimental models are needed to assess the innate immune response and evaluate emerging therapeutics.
The study presents a highly efficient, high-throughput murine model of AMI via LAD ligation without mechanical ventilation, enabling detailed temporal analysis of the innate immune response and cardiac remodeling.
Does not alter clinical AMI management; extends preclinical tools for temporal immune analysis in murine infarction.
The reduction in mortality following acute myocardial infarction (AMI) is an important achievement of modern medicine. Despite this progress, AMI remains the most common cause of heart failure (HF) and HF-related morbidity and mortality. The involvement of the innate immune response in different stages after AMI has at tracted important attention in recent years. With the increasing range of potential therapeutic compounds and delivery vectors, the need of highly efficient experimental AMI models is increasing, to support further advancement in this field. Here, we present a high-throughput model for the assessment of the innate immune response to AMI. The model is based on permanent surgical ligation of the left descending coronary artery (LAD) in mice, followed by complex flow-cytometry and histological analyses of immune cellular populations in blood and myocardium. We are presenting time-dependent qualitative and quantitative analysis results, demonstrating intense accumulation of Ly6G hi neutrophils and Ly6C hi monocytes in the infarcted myocardium on days 1 and 3 post-AMI, followed by successive accumulation of reparatory Ly6C lo MerTK hi macrophages, neovascularization and fibrosis development by day 7.
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Mareş et al. (2021) studied this question.
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