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.

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

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.

scholarly journals Role of Selected miRNAs as Diagnostic and Prognostic Biomarkers in Cardiovascular Diseases, Including Coronary Artery Disease, Myocardial Infarction and Atherosclerosis

2021 ◽  
Vol 8 (2) ◽  
pp. 22
Author(s):  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Naina Khullar ◽  
Ajaz Ahmad Waza ◽  
Chandan Jha ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
Cardiac Dysfunction ◽  
Heart Diseases ◽  
Prognostic Biomarkers ◽  
Apoptotic Bodies ◽  
Artery Disease

Cardiovascular diseases are the leading cause of death worldwide in different cohorts. It is well known that miRNAs have a crucial role in regulating the development of cardiovascular physiology, thus impacting the pathophysiology of heart diseases. MiRNAs also have been reported to be associated with cardiac reactions, leading to myocardial infarction (MCI) and ultimately heart failure (HF). To prevent these heart diseases, proper and timely diagnosis of cardiac dysfunction is pivotal. Though there are many symptoms associated with an irregular heart condition and though there are some biomarkers available that may indicate heart disease, authentic, specific and sensitive markers are the need of the hour. In recent times, miRNAs have proven to be promising candidates in this regard. They are potent biomarkers as they can be easily detected in body fluids (blood, urine, etc.) due to their remarkable stability and presence in apoptotic bodies and exosomes. Existing studies suggest the role of miRNAs as valuable biomarkers. A single biomarker may be insufficient to diagnose coronary artery disease (CAD) or acute myocardial infarction (AMI); thus, a combination of different miRNAs may prove fruitful. Therefore, this review aims to highlight the role of circulating miRNA as diagnostic and prognostic biomarkers in cardiovascular diseases such as coronary artery disease (CAD), myocardial infarction (MI) and atherosclerosis.

scholarly journals Role of the Cysteinyl Leukotrienes in the Pathogenesis and Progression of Cardiovascular Diseases

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Francesca Colazzo ◽  
Paolo Gelosa ◽  
Elena Tremoli ◽  
Luigi Sironi ◽  
Laura Castiglioni
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Diseases ◽  
Inflammatory Diseases ◽  
Asthma Management ◽  
Cardiovascular Disorders ◽  
Cysteinyl Leukotrienes ◽  
Pathway Activation ◽  
Cardioprotective Effects ◽  
Progression Of Atherosclerosis

Cysteinyl leukotrienes (CysLTs) are potent lipid inflammatory mediators synthesized from arachidonic acid, through the 5-lipoxygenase (5-LO) pathway. Owing to their properties, CysLTs play a crucial role in the pathogenesis of inflammation; therefore, CysLT modifiers as synthesis inhibitors or receptor antagonists, central in asthma management, may become a potential target for the treatment of other inflammatory diseases such as the cardiovascular disorders. 5-LO pathway activation and increased expression of its mediators and receptors are found in cardiovascular diseases. Moreover, the cardioprotective effects observed by using CysLT modifiers are promising and contribute to elucidate the link between CysLTs and cardiovascular disease. The aim of this review is to summarize the state of present research about the role of the CysLTs in the pathogenesis and progression of atherosclerosis and myocardial infarction.

scholarly journals Troponin: the biomarker of choice for the detection of cardiac injury

2005 ◽  
pp. 1191-1202
Author(s):  
Luciano Babuin ◽  
Allan S. Jaffe
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Troponin I ◽  
Cardiac Injury ◽  
Transaminase Activity ◽  
Elevated Troponin ◽  
Critical Issues ◽  
European Society Of Cardiology

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease. Troponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated.

Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction

2021 ◽  
Author(s):  
Andrew S Terker ◽  
Kensuke Sasaki ◽  
Juan Pablo Arroyo ◽  
Aolei Niu ◽  
Suwan Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ischemic Preconditioning ◽  
Renal Injury ◽  
Cardiac Injury ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Experimental Myocardial Infarction ◽  
Common Mechanism ◽  
Cardiac Damage ◽  
Chronic Kidney Injury

Ischemic heart disease is the leading cause of death worldwide and is frequently comorbid with chronic kidney disease. Physiological communication is known to occur between the heart and the kidney and primary dysfunction in either organ can induce dysfunction in the other, a clinical entity known as cardiorenal syndrome, but mechanistic details are lacking. Here, we used a model of experimental myocardial infarction (MI) to test effects of chronic cardiac ischemia on acute and chronic kidney injury. Surprisingly, chronic cardiac damage protected animals from subsequent acute ischemic renal injury, an effect that was accompanied by evidence of chronic kidney hypoxia. The protection observed post-MI was similar to protection observed in a separate group of healthy animals housed in ambient hypoxic conditions prior to kidney injury, suggesting a common mechanism. There was evidence that chronic cardiac injury activates renal hypoxia-sensing pathways. Increased renal abundance of several glycolytic enzymes following MI suggested a shift towards anaerobic glycolysis may confer renal ischemic preconditioning. In contrast, effects on chronic renal injury followed a different pattern with post-MI animals displaying worsened chronic renal injury and fibrosis. These data show that while chronic cardiac injury following MI protected against acute kidney injury via activation of hypoxia-sensing pathways, it worsened chronic kidney injury. The results further our understanding of cardiorenal signaling mechanisms and have implications for the treatment of heart failure patients with associated renal disease.

scholarly journals Emerging Roles for Immune Cells and MicroRNAs in Modulating the Response to Cardiac Injury

2019 ◽  
Vol 6 (1) ◽  
pp. 5 ◽  
Author(s):  
Adriana Rodriguez ◽  
Viravuth Yin
Keyword(s):  
Immune Cells ◽  
Cardiac Tissue ◽  
Heart Function ◽  
Cardiac Injury ◽  
Scar Tissue ◽  
Acute Injury ◽  
Heart Regeneration ◽  
Cardiomyocyte Proliferation ◽  
Cardiac Damage ◽  
Dynamic Interplay

Stimulating cardiomyocyte regeneration after an acute injury remains the central goal in cardiovascular regenerative biology. While adult mammals respond to cardiac damage with deposition of rigid scar tissue, adult zebrafish and salamander unleash a regenerative program that culminates in new cardiomyocyte formation, resolution of scar tissue, and recovery of heart function. Recent studies have shown that immune cells are key to regulating pro-inflammatory and pro-regenerative signals that shift the injury microenvironment toward regeneration. Defining the genetic regulators that control the dynamic interplay between immune cells and injured cardiac tissue is crucial to decoding the endogenous mechanism of heart regeneration. In this review, we discuss our current understanding of the extent that macrophage and regulatory T cells influence cardiomyocyte proliferation and how microRNAs (miRNAs) regulate their activity in the injured heart.

scholarly journals PENINGKATAN HIGH-SENSITIVE CARDIAC TROPONIN (HS-CTN) SETELAH LATIHAN INTENSITAS TINGGI YANG INTENSIF

2019 ◽  
Author(s):  
Indira Vidiari J ◽  
Nila Wahyuni ◽  
I Putu Adiartha Griadhi
Keyword(s):  
High Intensity ◽  
Cardiac Troponin ◽  
Meta Analysis ◽  
Cardiac Injury ◽  
High Sensitivity ◽  
Cardiac Damage ◽  
Intensive Exercise ◽  
Different Types ◽  
Underlying Pathophysiology

ABSTRACTThe role of exercise as a strategy for prevention, management and therapy in cardiovascular disease has been well described, but in some studies, it has been suggested that there is an increase in biomarkers in cardiac damage or cardiac troponin (cTn) after intensive, high-intensity exercise in healthy individuals. Several studies have shown significant increases in cardiac troponins after different types of exercise. The latest meta-analysis, showing that high-sensitivity cardiac troponin (hs-cTn) increases in about 83% of individuals after long and intensive exercise. The current pathophysiology of hs-cTn is not well understood. Several hypotheses have been proposed, such as transmembrane leakage from cytoplasmic free cTnT and cTnI or decreased troponin clearance from plasma, both caused by overloading of free radicals, myocardial stretching, elevated core temperature, or alteration of pH. Further research is needed with a full prospective study to evaluate the underlying pathophysiology of enhancing high sentivity cardiac troponin (hs-cTn) is an effective strategy for preventing or limiting cardiac injury and sport exercise safe for heart.Keywords: cardiac Troponin (cTn), high sensitivity cardiac troponin (hs-cTn), high intensity intensive exercise

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 Exercise Training on Autonomic Changes and Inflammatory Profile Induced by Myocardial Infarction

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Bruno Rodrigues ◽  
Fabio S. Lira ◽  
Fernanda M. Consolim-Colombo ◽  
Juraci A. Rocha ◽  
Erico C. Caperuto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mortality Rate ◽  
Exercise Training ◽  
Autonomic Imbalance ◽  
Pathological Conditions ◽  
Autonomic Changes ◽  
Immunological Changes ◽  
Inflammatory Profile ◽  
Parasympathetic Function

The cardiovascular autonomic imbalance in patients after myocardial infarction (MI) provides a significant increase in mortality rate, and seems to precede metabolic, hormonal, and immunological changes. Moreover, the reduction in the parasympathetic function has been associated with inflammatory response in different pathological conditions. Over the years, most of the studies have indicated the exercise training (ET) as an important nonpharmacological tool in the management of autonomic dysfunction and reduction in inflammatory profile after a myocardial infarction. In this work, we reviewed the effects of ET on autonomic imbalance after MI, and its consequences, particularly, in the post-MI inflammatory profile. Clinical and experimental evidence regarding relationship between alterations in autonomic regulation and local or systemic inflammation response after MI were also discussed.

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