Role of the immune system in cardiac tissue damage and repair following myocardial infarction

2017 ◽  
Vol 66 (9) ◽  
pp. 739-751 ◽  
Author(s):  
Arman Saparov ◽  
Vyacheslav Ogay ◽  
Talgat Nurgozhin ◽  
William C. W. Chen ◽  
Nurlan Mansurov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Tissue Damage ◽  
Cardiac Tissue

Involvement of monocytes/macrophages as key factors in the development and progression of cardiovascular diseases

2014 ◽  
Vol 458 (2) ◽  
pp. 187-193 ◽  
Author(s):  
María Fernández-Velasco ◽  
Silvia González-Ramos ◽  
Lisardo Boscá
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Cardiovascular Diseases ◽  
Cardiac Tissue ◽  
Initial Period ◽  
Cardiac Injury ◽  
Key Factors ◽  
Cardiac Damage ◽  
Inflammatory Profile

Emerging evidence points to the involvement of specialized cells of the immune system as key drivers in the pathophysiology of cardiovascular diseases. Monocytes are an essential cell component of the innate immune system that rapidly mobilize from the bone marrow to wounded tissues where they differentiate into macrophages or dendritic cells and trigger an immune response. In the healthy heart a limited, but near-constant, number of resident macrophages have been detected; however, this number significantly increases during cardiac damage. Shortly after initial cardiac injury, e.g. myocardial infarction, a large number of macrophages harbouring a pro-inflammatory profile (M1) are rapidly recruited to the cardiac tissue, where they contribute to cardiac remodelling. After this initial period, resolution takes place in the wound, and the infiltrated macrophages display a predominant deactivation/pro-resolution profile (M2), promoting cardiac repair by mediating pro-fibrotic responses. In the present review we focus on the role of the immune cells, particularly in the monocyte/macrophage population, in the progression of the major cardiac pathologies myocardial infarction and atherosclerosis.

Molecular Understanding of the Cardiomodulation in Myocardial Infarction and the Mechanism of Vitamin E Protections

2019 ◽  
Vol 19 (17) ◽  
pp. 1407-1426 ◽  
Author(s):  
Khairul Anwar Zarkasi ◽  
Tan Jen-Kit ◽  
Zakiah Jubri
Keyword(s):  
Myocardial Infarction ◽  
Vitamin E ◽  
Tissue Damage ◽  
Molecular Mechanisms ◽  
Cardiac Tissue ◽  
Ppar Γ ◽  
Intracellular Signalling Pathways ◽  
Survival Pathways ◽  
Cause Of Deaths

: Myocardial infarction is a major cause of deaths globally. Modulation of several molecular mechanisms occurs during the initial stages of myocardial ischemia prior to permanent cardiac tissue damage, which involves both pathogenic as well as survival pathways in the cardiomyocyte. Currently, there is increasing evidence regarding the cardioprotective role of vitamin E in alleviating the disease. This fat-soluble vitamin does not only act as a powerful antioxidant; but it also has the ability to regulate several intracellular signalling pathways including HIF-1, PPAR-γ, Nrf-2, and NF-κB that influence the expression of a number of genes and their protein products. Essentially, it inhibits the molecular progression of tissue damage and preserves myocardial tissue viability. This review aims to summarize the molecular understanding of the cardiomodulation in myocardial infarction as well as the mechanism of vitamin E protection.

scholarly journals Apoptosis Modulation in the Immune System Reveals a Role of Neutrophils in Tissue Damage in a Murine Model of Chlamydial Genital Infection

2018 ◽  
Vol 217 (11) ◽  
pp. 1832-1843
Author(s):  
Tom Zortel ◽  
Annette Schmitt-Graeff ◽  
Susanne Kirschnek ◽  
Georg Häcker
Keyword(s):  
Immune System ◽  
Murine Model ◽  
Tissue Damage ◽  
Genital Infection

scholarly journals 0375: Re-evaluation of the role of mast cell in cardiac tissue following myocardial infarction

2014 ◽  
Vol 6 ◽  
pp. 28
Author(s):  
Anta Ngkelo ◽  
Adele Richart ◽  
Jose Vilar ◽  
Pauline Marck ◽  
Christophe Heymes ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mast Cell ◽  
Cardiac Tissue

scholarly journals Immunopharmacology of Post-Myocardial Infarction and Heart Failure Medications

2018 ◽  
Vol 7 (11) ◽  
pp. 403 ◽  
Author(s):  
Mona Panahi ◽  
Nimai Vadgama ◽  
Mathun Kuganesan ◽  
Fu Ng ◽  
Susanne Sattler
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Immune Response ◽  
Immune System ◽  
Tissue Damage ◽  
Heart Function ◽  
The Body ◽  
Inflammatory Conditions ◽  
Drug Classes ◽  
Potential Benefits

The immune system responds to acute tissue damage after myocardial infarction (MI) and orchestrates healing and recovery of the heart. However, excessive inflammation may lead to additional tissue damage and fibrosis and exacerbate subsequent functional impairment, leading to heart failure. The appreciation of the immune system as a crucial factor after MI has led to a surge of clinical trials investigating the potential benefits of immunomodulatory agents previously used in hyper-inflammatory conditions, such as autoimmune disease. While the major goal of routine post-MI pharmacotherapy is to support heart function by ensuring appropriate blood pressure and cardiac output to meet the demands of the body, several drug classes also affect a range of immunological pathways and modulate the post-MI immune response, which is crucial to take into account when designing future immunomodulatory trials. This review outlines how routine post-MI pharmacotherapy affects the immune response and may thus influence post-MI outcomes and development towards heart failure. Current key drug classes are discussed, including platelet inhibitors, statins, β-blockers, and renin–angiotensin–aldosterone inhibitors.

scholarly journals Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 51
Author(s):  
William P. Lafuse ◽  
Daniel J. Wozniak ◽  
Murugesan V. S. Rajaram
Keyword(s):  
Tissue Damage ◽  
Tissue Repair ◽  
Cardiac Tissue ◽  
Tissue Injury ◽  
The Body ◽  
T And B Cells ◽  
Functional Changes ◽  
Cardiac Inflammation ◽  
And Function

The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been conventionally described as a disease associated with cardiac tissue damage caused by systemic inflammation, arrhythmia and conduction defects. Cardiac inflammation and subsequent tissue damage is orchestrated by the infiltration and activation of various immune cells including neutrophils, monocytes, macrophages, eosinophils, mast cells, natural killer cells, and T and B cells into the myocardium. After tissue injury, monocytes and tissue-resident macrophages undergo marked phenotypic and functional changes, and function as key regulators of tissue repair, regeneration and fibrosis. Disturbance in resident macrophage functions such as uncontrolled production of inflammatory cytokines, growth factors and inefficient generation of an anti-inflammatory response or unsuccessful communication between macrophages and epithelial and endothelial cells and fibroblasts can lead to aberrant repair, persistent injury, and HF. Therefore, in this review, we discuss the role of cardiac macrophages on cardiac inflammation, tissue repair, regeneration and fibrosis.

scholarly journals Targeting Inflammation after Myocardial Infarction: A Therapeutic Opportunity for Extracellular Vesicles?

2021 ◽  
Vol 22 (15) ◽  
pp. 7831
Author(s):  
Margarida Viola ◽  
Saskia C. A. de Jager ◽  
Joost P. G. Sluijter
Keyword(s):  
Myocardial Infarction ◽  
Immune System ◽  
Extracellular Vesicles ◽  
Cardiac Inflammation ◽  
Stem And Progenitor Cells ◽  
Therapeutic Opportunity ◽  
Strong Inflammatory Response ◽  
Non Coding Rnas ◽  
Dead Tissue

After myocardial infarction (MI), a strong inflammatory response takes place in the heart to remove the dead tissue resulting from ischemic injury. A growing body of evidence suggests that timely resolution of this inflammatory process may aid in the prevention of adverse cardiac remodeling and heart failure post-MI. The present challenge is to find a way to stimulate this process without interfering with the reparative role of the immune system. Extracellular vesicles (EVs) are natural membrane particles that are released by cells and carry different macromolecules, including proteins and non-coding RNAs. In recent years, EVs derived from various stem and progenitor cells have been demonstrated to possess regenerative properties. They can provide cardioprotection via several mechanisms of action, including immunomodulation. In this review, we summarize the role of the innate immune system in post-MI healing. We then discuss the mechanisms by which EVs modulate cardiac inflammation in preclinical models of myocardial injury through regulation of monocyte influx and macrophage function. Finally, we provide suggestions for further optimization of EV-based therapy to improve its potential for the treatment of MI.

scholarly journals The Role of the Intestinal Context in the Generation of Tolerance and Inflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Bernardo Sgarbi Reis ◽  
Daniel Mucida
Keyword(s):  
Immune System ◽  
Health Status ◽  
Tissue Damage ◽  
Lymphoid Tissue ◽  
Pathogenic Bacteria ◽  
The Body ◽  
Regulatory Mechanisms ◽  
System A ◽  
Enormous Amount

The mucosal surface of the intestine alone forms the largest area exposed to exogenous antigens as well as the largest collection of lymphoid tissue in the body. The enormous amount of nonpathogenic and pathogenic bacteria and food-derived antigens that we are daily exposed sets an interesting challenge to the immune system: a protective immune activity must coexist with efficient regulatory mechanisms in order to maintain a health status of these organisms. This paper discusses how the immune system assimilates the perturbations from the environment without generating tissue damage.

Sign in / Sign up

Export Citation Format

Share Document