The role of anti-myosin antibodies in perpetuating cardiac damage following myocardial infarction

2016 ◽  
Vol 209 ◽  
pp. 226-233 ◽  
Author(s):  
Tom J. O'Donohoe ◽  
Ryan G. Schrale ◽  
Natkunam Ketheesan
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Damage

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.

Effect of vitamin D on isoprenaline-induced myocardial infarction in rats: possible role of peroxisome proliferator-activated receptor-γ

2017 ◽  
Vol 95 (6) ◽  
pp. 641-646 ◽  
Author(s):  
Ola Ahmed El-Gohary ◽  
Mona Maher Allam
Keyword(s):  
Myocardial Infarction ◽  
Vitamin D ◽  
Diglycidyl Ether ◽  
Peroxisome Proliferator ◽  
Oxidative Stress Biomarkers ◽  
Cardiac Damage ◽  
Necrosis Factor Alpha ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ

Infarct-like lesion induced by isoprenaline is a well-known model to study myocardial infarction (MI). Vitamin D has been shown to have anti-inflammatory and antioxidant effects. Recent studies highlighted cross talk between vitamin D and peroxisome proliferator-activated receptor gamma (PPAR-γ). The present study was designed to investigate the effect of pretreatment with vitamin D on the isoprenaline-induced infarct-like lesion in rats and the role of PPAR-γ as a novel mechanism in vitamin-D-mediated cardioprotective effect. Markers chosen to assess cardiac damage included serum level of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). Cardiac contents of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH) were also assessed. Furthermore, ECG monitoring and measurement of injury extension were carried out. Isoprenaline increased the level of cardiac enzymes, as well as inflammatory and oxidative stress biomarkers. In addition, it produced ST-segment elevation. Pretreatment with vitamin D significantly improved previous parameters. The prior treatment with bisphenol A diglycidyl ether (BADGE), a PPAR-γ antagonist, significantly attenuated the protective effect of vitamin D. In conclusion, vitamin D can be demonstrated as a promising cardioprotective agent in MI and PPAR-γ significantly contributes toward vitamin-D-mediated protection.

scholarly journals Role of Androgens in Sex Differences in Cardiac Damage During Myocardial Infarction

Endocrinology ◽  
2014 ◽  
Vol 155 (2) ◽  
pp. 568-575 ◽  
Author(s):  
Thi Y. L. Le ◽  
Anthony W. Ashton ◽  
Mahidi Mardini ◽  
Peter G. Stanton ◽  
John W. Funder ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sex Differences ◽  
Androgen Receptor ◽  
Sex Steroids ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
B Cell Lymphoma ◽  
Male Rats ◽  
Cardiac Damage

Age-specific incidence of ischemic heart disease in men is higher than in women, although women die more frequently without previous symptoms; the molecular mechanism(s) are poorly understood. Most studies focus on protection by estrogen, with less attention on androgen receptor-mediated androgen actions. Our aim was to determine the role of androgens in the sex differences in cardiac damage during myocardial infarction. Mature age-matched male and female Sprague Dawley rats, intact or surgically gonadectomized (Gx), received testosterone (T) or 17β-estradiol (E2) via subdermal SILASTIC (Dow Corning Corp.) implants; a subset of male rats received dihydrotestosterone. After 21 days, animals were anesthetized, and hearts were excised and subjected to ex vivo regional ischemia-reperfusion (I-R). Hearts from intact males had larger infarcts than those from females following I-R; Gx produced the opposite effect, confirming a role for sex steroids. In Gx males, androgens (dihydrotestosterone, T) and E2 aggravated I-R-induced cardiac damage, whereas in Gx females, T had no effect and E2 reduced infarct area. Increased circulating T levels up-regulated androgen receptor and receptor for advanced glycation end products, which resulted in enhanced apoptosis aggravating cardiac damage in both males and females. In conclusion, our study demonstrates, for the first time, that sex steroids regulate autophagy during myocardial infarction and shows that a novel mechanism of action for androgens during I-R is down-regulation of antiapoptotic protein Bcl-xL (B cell lymphoma-extra large), a key controller for cross talk between autophagy and apoptosis, shifting the balance toward apoptosis and leading to aggravated cardiac damage.

scholarly journals Exosomes and myocardial infarction: scientific and practical interest

2021 ◽  
Vol 38 (4) ◽  
pp. 76-84
Author(s):  
O. V. Khlynova ◽  
R. A. Rodionov ◽  
N. S. Karpunina ◽  
E. A. Shishkina
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Response ◽  
Practical Interest ◽  
Biological Information ◽  
Cardiac Damage ◽  
Intercellular Transport ◽  
Pathological Conditions ◽  
Damage Repair ◽  
Strong Inflammatory Response

A review of the literature on the biological role of exosomes in the pathophysiology of a number of pathological conditions, including damage to the heart muscle in the variant of myocardial infarction (MI), is presented. In the last decade, exosomes have begun to be actively studied; a lot of data have appeared on their nature and role in intercellular transport and signaling both in normal conditions and in pathology. Exosomes are important carriers of biological information, facilitating intercellular communication and participating in the pathophysiology of various cardiovascular diseases. In myocardial infarction, massive cardiomyocyte death triggers a strong inflammatory response, which is a vital process for cardiac damage, repair, and remodeling. A growing body of evidence suggests that exosomes are involved in the inflammatory response and immune regulation after MI.

scholarly journals New Insights and Novel Therapeutic Potentials for Macrophages in Myocardial Infarction

Inflammation ◽  
2021 ◽  
Author(s):  
Zenglei Zhang ◽  
Junnan Tang ◽  
Xiaolin Cui ◽  
Bo Qin ◽  
Jianchao Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Therapeutic Potential ◽  
Cardiac Injury ◽  
Early Period ◽  
Cardiac Damage ◽  
Overwhelming Evidence ◽  
Classically Activated Macrophages ◽  
And Function ◽  
Alternatively Activated

Abstract Cardiovascular disease (CVD) has long been the leading cause of death worldwide, and myocardial infarction (MI) accounts for the greatest proportion of CVD. Recent research has revealed that inflammation plays a major role in the pathogenesis of CVD and other manifestations of atherosclerosis. Overwhelming evidence supports the view that macrophages, as the basic cell component of the innate immune system, play a pivotal role in atherosclerosis initiation and progression. Limited but indispensable resident macrophages have been detected in the healthy heart; however, the number of cardiac macrophages significantly increases during cardiac injury. In the early period of initial cardiac damage (e.g., MI), numerous classically activated macrophages (M1) originating from the bone marrow and spleen are rapidly recruited to damaged sites, where they are responsible for cardiac remodeling. After the inflammatory stage, the macrophages shift toward an alternatively activated phenotype (M2) that promotes cardiac repair. In addition, extensive studies have shown the therapeutic potential of macrophages as targets, especially for emerging nanoparticle-mediated drug delivery systems. In the present review, we focused on the role of macrophages in the development and progression of MI, factors regulating macrophage activation and function, and the therapeutic potential of macrophages in MI.

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