Innate Immune Mechanisms in Myocardial Infarction - An Update

Mareş, Răzvan Gheorghiţă; Marinković, Goran; Cotoi, Ovidiu Simion; Schiopu, Alexandru

doi:10.1515/rrlm-2017-0031

Cited by 3 publications

(2 citation statements)

References 64 publications

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“…The local infl ammatory infi ltrate following an AMI has a crucial infl uence on both the size of the injury and on the effi ciency of the reparatory mechanisms that determine myocardial remodeling and post-AMI prognosis 24 . The myocardial ischemia followed by necrosis triggers a potent immune reaction involving two mechanistically distinct phases: the infl ammatory phase and the repa ratory phase 25 .…”

Section: Discussionmentioning

confidence: 99%

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

Mareş

Manu

Szabó

et al. 2021

Romanian Journal of Cardiology

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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 Ly6Ghi neutrophils and Ly6Chi monocytes in the infarcted myocardium on days 1 and 3 post-AMI, followed by successive accumulation of reparatory Ly6CloMerTKhi macrophages, neovascularization and fibrosis development by day 7.

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Section: Discussionmentioning

confidence: 99%

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

Mareş

Manu

Szabó

et al. 2021

Romanian Journal of Cardiology

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“…From a pathological standpoint, MI consists in myocardial cell death due to acute ischemia. Extensive cardiomyocyte death triggers a robust immune and inflammatory response that leads to myocardial healing and replacement of the damaged tissue with a collagen-based scar [ 2 , 3 ]. During acute cardiac inflammation, high numbers of immune cells infiltrate the myocardium and initially exacerbate tissue damage, before conversion into a reparatory phenotype.…”

Section: Introductionmentioning

confidence: 99%

S100A8/A9 is a valuable biomarker and treatment target to detect and modulate neutrophil involvement in myocardial infarction

Mareş¹,

Sabău²,

Cocuz³

et al. 2023

Rom J Morphol Embryol

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Myocardial infarction (MI) leads to irreversible ischemic damage of the heart muscle and is the leading cause of heart failure. The ischemic cardiac injury triggers a potent local and systemic immune response. In the acute phase post-MI, neutrophils infiltrate the myocardium in large numbers and induce further cardiomyocyte death, expanding the infarcted area. The alarmin S100A8/A9 is a proinflammatory mediator primarily produced by myeloid cells, with an emerging role in MI. We previously demonstrated that short-term inhibition of S100A8/A9 during the inflammatory phase of the immune response to MI improves long-term cardiac function. In the present study, we investigated the effects of S100A8/A9 blockade on myocardial inflammation and post-ischemic myocardial injury in a mouse model of coronary artery ligation. Immunohistochemical (IHC) staining revealed that the presence of S100A9 is strongly correlated with neutrophil infiltration in the myocardium on days 1 and 3 post-MI. A 3-day treatment with the S100A8/A9 blocker ABR-238901 starting immediately after MI decreased the number of neutrophils and S100A9 presence in the myocardium and had a positive impact on cardiac damage, reducing infarction size. These findings promote S100A9 as an IHC biomarker of neutrophil infiltration and a promising immunomodulatory target to regulate neutrophil recruitment, reduce ischemic injury and promote long-term beneficial cardiac recovery after MI.

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Neutrophil-to-Lymphocyte Ratio – Risk of Amputation and Mortality in Patients with Limb-Threatening Ischemia – a Systematic Review

Lăpădatu,

Russu

2024

Journal of Cardiovascular Emergencies

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Acute limb ischemia (ALI) and chronic limb-threatening ischemia (CLTI) are severe vascular conditions that can be lethal. The inflammatory response in these diseases, characterized by increased levels of neutrophils and platelets, highlights the importance of prompt management. The neutrophil-to-lymphocyte ratio (NLR) has emerged as a useful biomarker during the COVID-19 pandemic and high NLR levels were found to be associated with an increased risk of ALI and other thromboembolic events. The aim of this systematic review was to analyze the prognostic role of the NLR regarding the risk of amputation and mortality in patients diagnosed with ALI and CLTI. We included 12 studies (five for ALI, with 1,145 patients, and seven for CLTI, with 1,838 patients), following the PRISMA guidelines. Treatment results were evaluated, including amputation and mortality. We found that high NLR values were consistently associated with an increased risk of amputation and/or mortality, with pooled odds ratios ranging from 1.28 to 11.09 in patients with ALI and from 1.97 to 5.6 in patients with CLTI. The results suggest that NLR may represent an important tool for informed decision-making in the management of these patients.

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Innate Immune Mechanisms in Myocardial Infarction - An Update

Abstract: Acute myocardial infarction (AMI) is a disease associated with high morbidity and mortality. Currently there

Cited by 3 publications

References 64 publications

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

Studying the Innate Immune Response to Myocardial Infarction in a Highly Efficient Experimental Animal Model

S100A8/A9 is a valuable biomarker and treatment target to detect and modulate neutrophil involvement in myocardial infarction

Neutrophil-to-Lymphocyte Ratio – Risk of Amputation and Mortality in Patients with Limb-Threatening Ischemia – a Systematic Review

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