Role of Toll-like receptors in cardiovascular diseases

2011 ◽  
Vol 121 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Jesus G. Vallejo
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Viral Myocarditis ◽  
Left Ventricular ◽  
Innate Immune ◽  
Present Review ◽  
Cardiac Remodelling ◽  
Septic Cardiomyopathy ◽  
Immune Recognition

The discovery and characterization of the TLR (Toll-like receptor) family has led to a better understanding of the innate immune system. The strategy of innate immune recognition is based on the detection of constitutive and conserved products of micro-organisms. However, host molecules that are released during injury can also activate TLRs. Engagement of TLRs by microbial or host-derived molecules induces the expression of pro-inflammatory cytokines, which may have both beneficial and detrimental effects on the host. In addition to being expressed in immune cells, TLRs are expressed in other tissues such as those of the cardiovascular system. In the present review, the role of TLRs in septic cardiomyopathy, viral myocarditis, atherosclerosis, ischaemia/reperfusion injury and cardiac remodelling after myocardial infarction are outlined, with attention paid to genetically modified murine models. Although much has been learned about stress-induced TLR activation in the tissues of the cardiovascular system, the role of individual TLRs in initiating and integrating homoeostatic responses within the heart remains to be defined. Accumulating evidence indicates that TLRs may play an important role in the pathogenesis of atherosclerosis, viral myocarditis, dilated cardiomyopathy, cardiac allograft rejection and sepsis-induced left ventricular dysfunction. Moreover, heart failure of diverse aetiology is also now recognized to have an important immune component, with TLR signalling influencing the process of cardiac remodelling and prognosis. In the present review, we outline the biology of TLRs as well as the current experimental and clinical evidence for the role of TLRs in cardiovascular diseases.

scholarly journals microRNAs in the onset and development of cardiovascular disease

2013 ◽  
Vol 126 (3) ◽  
pp. 183-194 ◽  
Author(s):  
Kasey C. Vickers ◽  
Kerry-Anne Rye ◽  
Fatiha Tabet
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Present Review ◽  
Novel Therapies ◽  
Regulatory Processes ◽  
Gene Regulatory

Physiological and pathological roles for small non-encoding miRNAs (microRNAs) in the cardiovascular system have recently emerged and are now widely studied. The discovery of widespread functions of miRNAs has increased the complexity of gene-regulatory processes and networks in both the cardiovascular system and cardiovascular diseases. Indeed, it has recently been shown that miRNAs are implicated in the regulation of many of the steps leading to the development of cardiovascular disease. These findings represent novel aspects in miRNA biology and, therefore, our understanding of the role of these miRNAs during the pathogenesis of cardiovascular disease is critical for the development of novel therapies and diagnostic interventions. The present review will focus on understanding how miRNAs are involved in the onset and development of cardiovascular diseases.

scholarly journals Differential Role of Leptin and Adiponectin in Cardiovascular System

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
C. M. Ghantous ◽  
Z. Azrak ◽  
S. Hanache ◽  
W. Abou-Kheir ◽  
A. Zeidan
Keyword(s):  
Cardiovascular Diseases ◽  
Left Ventricular Hypertrophy ◽  
Cardiovascular System ◽  
Ventricular Hypertrophy ◽  
Population Based ◽  
Left Ventricular ◽  
Tissue Mass ◽  
Cross Sectional

Leptin and adiponectin are differentially expressed adipokines in obesity and cardiovascular diseases. Leptin levels are directly associated with adipose tissue mass, while adiponectin levels are downregulated in obesity. Although significantly produced by adipocytes, leptin is also produced by vascular smooth muscle cells and cardiomyocytes. Plasma leptin concentrations are elevated in cases of cardiovascular diseases, such as hypertension, congestive heart failure, and myocardial infarction. As for the event of left ventricular hypertrophy, researchers have been stirring controversy about the role of leptin in this form of cardiac remodeling. In this review, we discuss how leptin has been shown to play an antihypertrophic role in the development of left ventricular hypertrophy throughin vitroexperiments, population-based cross-sectional studies, and longitudinal cohort studies. Conversely, we also examine how leptin may actually promote left ventricular hypertrophy usingin vitroanalysis and human-based univariate and multiple linear stepwise regression analysis. On the other hand, as opposed to leptin’s generally detrimental effects on the cardiovascular system, adiponectin is a cardioprotective hormone that reduces left ventricular and vascular hypertrophy, oxidative stress, and inflammation. In this review, we also highlight adiponectin signaling and its protective actions on the cardiovascular system.

scholarly journals Role of the Innate Immune System in Acute Viral Myocarditis

2009 ◽  
Vol 104 (3) ◽  
pp. 228-237 ◽  
Author(s):  
Chien-Hua Huang ◽  
Jesus G. Vallejo ◽  
George Kollias ◽  
Douglas L. Mann
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Viral Myocarditis ◽  
Innate Immune ◽  
Acute Viral Myocarditis

scholarly journals The role of systemic inflammation in heart failure

2021 ◽  
Vol 102 (4) ◽  
pp. 510-517
Author(s):  
E V Khazova ◽  
O V Bulashova
Keyword(s):  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Systemic Inflammation ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
C Reactive Protein ◽  
Ventricular Ejection Fraction ◽  
Reactive Protein ◽  
Highly Sensitive

The discussion continues about the role of systemic inflammation in the pathogenesis of cardiovascular diseases of ischemic etiology. This article reviews the information on the role of C-reactive protein in patients with atherosclerosis and heart failure in risk stratification for adverse cardiovascular events, including assessment of factors affecting the basal level of highly sensitive C-reactive protein. Research data (MRFIT, MONICA) have demonstrated a relationship between an increased level of C-reactive protein and the development of coronary heart disease. An increase in the serum level of highly sensitive C-reactive protein is observed in arterial hypertension, dyslipidemia, type 2 diabetes mellitus and insulin resistance, which indicates the involvement of systemic inflammation in these disorders. Currently, the assessment of highly sensitive C-reactive protein is used to determine the risk of developing myocardial infarction and stroke. It has been proven that heart failure patients have a high level of highly sensitive C-reactive protein compared with patients without heart failure. The level of C-reactive protein is referred to as modifiable risk factors for cardiovascular diseases of ischemic origin, since lifestyle changes or taking drugs such as statins, non-steroidal anti-inflammatory drugs, glucocorticoids, etc. reduce the level of highly sensitive C-reactive protein. In patients with heart failure with different left ventricular ejection fraction values, it was found that the regression of the inflammatory response is accompanied by an improvement in prognosis, which confirms the hypothesis of inflammation as a response to stress, which has negative consequences for the cardiovascular system.

Role of gp91phox-containing NADPH oxidase in left ventricular remodeling induced by intermittent hypoxic stress

2008 ◽  
Vol 294 (5) ◽  
pp. H2197-H2203 ◽  
Author(s):  
Tetsuya Hayashi ◽  
Chika Yamashita ◽  
Chika Matsumoto ◽  
Chol-Jun Kwak ◽  
Kiwako Fujii ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Nadph Oxidase ◽  
Intermittent Hypoxia ◽  
Sleep Apnea Syndrome ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Hypoxic Stress ◽  
Wild Type ◽  
Lv Remodeling

Intermittent hypoxia due to sleep apnea syndrome is associated with cardiovascular diseases. However, the precise mechanisms by which intermittent hypoxic stress accelerates cardiovascular diseases are largely unclear. The aim of this study was to investigate the role of gp91 phox-containing NADPH oxidase in the development of left ventricular (LV) remodeling induced by intermittent hypoxic stress in mice. Male gp91 phox-deficient (gp91−/−) mice ( n = 26) and wild-type ( n = 39) mice at 7–12 wk of age were exposed to intermittent hypoxia (30 s of 4.5–5.5% O2 followed by 30 s of 21% O2 for 8 h/day during daytime) or normoxia for 10 days. Mean blood pressure and LV systolic and diastolic function were not changed by intermittent hypoxia in wild-type or gp91−/− mice, although right ventricular systolic pressure tended to be increased. In wild-type mice, intermittent hypoxic stress significantly increased the diameter of cardiomyocytes and interstitial fibrosis in LV myocardium. Furthermore, intermittent hypoxic stress increased superoxide production, 4-hydroxy-2-nonenal protein, TNF-α and transforming growth factor-β mRNA, and NF-κB binding activity in wild-type, but not gp91−/−, mice. These results suggest that gp91 phox-containing NADPH oxidase plays a crucial role in the pathophysiology of intermittent hypoxia-induced LV remodeling through an increase of oxidative stress.

scholarly journals Cardiovascular system status of long-livers in Moscow: the prevalence of cardiovascular diseases and their risk factors

2021 ◽  
Vol 26 ◽  
pp. 4028
Author(s):  
K. A. Eruslanova ◽  
A. V. Luzina ◽  
Yu. S. Onuchina ◽  
V. S. Ostapenko ◽  
N. V. Sharashkina ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
Interventricular Septum ◽  
Systolic Heart Failure ◽  
Left Ventricular ◽  
Past Century ◽  
Cvd Risk Factors ◽  
Cvd Risk

Over the past century, an increase in life expectancy has been observed in Russia and in the world. According to the United Nations, by 2100, the number of centenarians worldwide will reach 25 million. Despite the annual increase in the number of super-centenarians, this age group remains poorly understood.Aim. To estimate the prevalence of cardiovascular diseases (CVD) and the main risk factors among super-centenarians in Moscow.Material and methods. According to the register of long-livers in Moscow, 82 people aged 95 to 105 were included. Participants were examined at home.The history of life and the presence of chronic diseases was collected by participant words. To assess the state of cardiovascular system, an ultrasound of the heart and main arteries was performed.Results. Conventional CVD risk factors were the exception rather than the rule among study participants (smoking — 8 patients (9,8%), alcohol abuse — 4 (4,9%), obesity — 6 (7,3%)). Dyslipidemia was relatively widespread (n=37; 45,1%), however, there were no pronounced abnormalities in the lipid profile: the maximum increase in low-density lipoproteins was 5,6 mmol/L. The most common CVDs among the participants were hypertension (n=64; 78%), coronary artery disease (n=42; 51,2%), and heart failure (n=26; 31,7%); other diseases were much less common. The most common echocardiographic changes were left atrial dilatation (n=38; 74,5%), increased left ventricular mass, thickening of left ventricular posterior wall (n=24; 48%) and interventricular septum (n=51; 100%). Diastolic and systolic heart failure were not widespread among long-livers: 16 (32%) and 2 (3,9%), respectively. Despite a rather large number of atherosclerotic plaques in the common carotid and femoral arteries, the number of hemodynamically significant plaques was low (n=3; 4,6%). An intima-media thickening up to 1,0-1,1 mm was found.Conclusion. Long-livers in Moscow are characterized by a low prevalence of traditional CVD risk factors (with the exception of hypertension) and a fairly high prevalence of atherosclerotic CVDs, which are characterized by a subclinical course.

scholarly journals Resolving the Ionotropic P2X4 Receptor Mystery Points towards a New Therapeutic Target for Cardiovascular Diseases

2020 ◽  
Vol 21 (14) ◽  
pp. 5005 ◽  
Author(s):  
Bruno Bragança ◽  
Paulo Correia-de-Sá
Keyword(s):  
Clinical Practice ◽  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
State Of The Art ◽  
P2x4 Receptor ◽  
Extracellular Milieu ◽  
Intracellular Energy ◽  
Further Development ◽  
Cardiovascular Functions

Adenosine triphosphate (ATP) is a primordial versatile autacoid that changes its role from an intracellular energy saver to a signaling molecule once released to the extracellular milieu. Extracellular ATP and its adenosine metabolite are the main activators of the P2 and P1 purinoceptor families, respectively. Mounting evidence suggests that the ionotropic P2X4 receptor (P2X4R) plays pivotal roles in the regulation of the cardiovascular system, yet further therapeutic advances have been hampered by the lack of selective P2X4R agonists. In this review, we provide the state of the art of the P2X4R activity in the cardiovascular system. We also discuss the role of P2X4R activation in kidney and lungs vis a vis their interplay to control cardiovascular functions and dysfunctions, including putative adverse effects emerging from P2X4R activation. Gathering this information may prompt further development of selective P2X4R agonists and its translation to the clinical practice.

scholarly journals Emerging role of VCP/p97 in cardiovascular diseases: novel insights and therapeutic opportunities

2021 ◽  
Author(s):  
Hongyang Shu ◽  
Yizhong Peng ◽  
Weijian Hang ◽  
Ning Zhou ◽  
Dao Wen Wang
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Reperfusion Injury ◽  
Cardiovascular System ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Therapeutic Potential ◽  
Ischemia Reperfusion ◽  
Heart Research

Valosin-containing protein (VCP/p97) is a member of the conserved type II AAA+ (ATPases associated with diverse cellular activities) family of proteins with multiple biological functions, especially in protein homeostasis. Mutations in VCP/p97 are reportedly related to unique autosomal dominant diseases, which may worsen cardiac function. Although the structure of VCP/p97 has been clearly characterized, with reports of high abundance in the heart, research focusing on the molecular mechanisms underpinning the roles of VCP/p97 in the cardiovascular system has been recently undertaken over the past decades. Recent studies have shown that VCP/p97 deficiency affects myocardial fibers and induces heart failure, while overexpression of VCP/p97 eliminates ischemia/reperfusion injury and relieves pathological cardiac hypertrophy caused by cardiac pressure overload, which is related to changes in the mitochondria and calcium overload. However, certain studies have drawn opposing conclusions, including the mitigation of ischemia/reperfusion injury via inhibition of VCP/p97 ATPase activity. Nevertheless, these emerging studies shed light on the role of VCP/p97 and its therapeutic potential in cardiovascular diseases. In other words, VCP/p97 may be involved in the development of cardiovascular disease, and is anticipated to be a new therapeutic target. This review summarizes current findings regarding VCP/p97 in the cardiovascular system for the first time, and discusses the role of VCP/p97 in cardiovascular disease.

scholarly journals Mitochondrial Transfer in Cardiovascular Disease: From Mechanisms to Therapeutic Implications

2021 ◽  
Vol 8 ◽  
Author(s):  
Jun Chen ◽  
Jinjie Zhong ◽  
Lin-lin Wang ◽  
Ying-ying Chen
Keyword(s):  
Cardiovascular Diseases ◽  
Cardiovascular System ◽  
System Development ◽  
Critical Role ◽  
Extracellular Vesicle ◽  
Therapeutic Implications ◽  
Pathological Conditions ◽  
Mitochondrial Transfer ◽  
Transfer Strategies

Mitochondrial dysfunction has been proven to play a critical role in the pathogenesis of cardiovascular diseases. The phenomenon of intercellular mitochondrial transfer has been discovered in the cardiovascular system. Studies have shown that cell-to-cell mitochondrial transfer plays an essential role in regulating cardiovascular system development and maintaining normal tissue homeostasis under physiological conditions. In pathological conditions, damaged cells transfer dysfunctional mitochondria toward recipient cells to ask for help and take up exogenous functional mitochondria to alleviate injury. In this review, we summarized the mechanism of mitochondrial transfer in the cardiovascular system and outlined the fate and functional role of donor mitochondria. We also discussed the advantage and challenges of mitochondrial transfer strategies, including cell-based mitochondrial transplantation, extracellular vesicle-based mitochondrial transplantation, and naked mitochondrial transplantation, for the treatment of cardiovascular disorders. We hope this review will provide perspectives on mitochondrial-targeted therapeutics in cardiovascular diseases.

Role of TRAF3 in neurological and cardiovascular diseases: an overview of recent studies

2017 ◽  
Vol 8 (3-4) ◽  
pp. 197-202 ◽  
Author(s):  
Natalia Cullell ◽  
Elena Muiño ◽  
Caty Carrera ◽  
Nuria Torres ◽  
Jerzy Krupinski ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Target Genes ◽  
Adaptor Protein ◽  
Innate Immune ◽  
Tumour Necrosis Factor Receptor ◽  
Transcriptional Level ◽  
Cell Type ◽  
Vascular Recurrence ◽  
Necrosis Factor

AbstractTumour necrosis factor receptor-associated factor 3 (TRAF3) is a member of the TRAF adaptor protein family, which exerts different effects on the cell depending on the receptor to which it binds and the cell type in which it is expressed. TRAF3 is a major regulator of the innate immune response. To perform its functions properly, TRAF3 is transcriptionally and epigenetically regulated. At the transcriptional level, TRAF3 expression has been associated with neurological and cardiovascular diseases including stroke, among other pathologies. Epigenetic modifications of TRAF3 have been observed at the histone and DNA levels. It has been observed that acetylation of TRAF3, as well as other NF-κβ target genes, is associated with cardiac hypertrophy. Furthermore, TRAF3 methylation has been associated with vascular recurrence after ischemic stroke in patients treated with clopidogrel. In this overview, we summarise the most interesting studies related to transcriptional and epigenetic regulation of TRAF3 focusing on those studies performed in neurological and cardiovascular diseases.

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