scholarly journals Inhibition of c-Src Tyrosine Kinase Prevents Angiotensin II–Mediated Connexin-43 Remodeling and Sudden Cardiac Death

2011 ◽  
Vol 58 (22) ◽  
pp. 2332-2339 ◽  
Author(s):  
Ali A. Sovari ◽  
Shahriar Iravanian ◽  
Elena Dolmatova ◽  
Zhe Jiao ◽  
Hong Liu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sudden Cardiac Death ◽  
Tyrosine Kinase ◽  
Cardiac Death ◽  
Connexin 43 ◽  
Src Tyrosine Kinase

scholarly journals Cardiac macrophages prevent sudden death during heart stress

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Junichi Sugita ◽  
Katsuhito Fujiu ◽  
Yukiteru Nakayama ◽  
Takumi Matsubara ◽  
Jun Matsuda ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Sudden Death ◽  
Gap Junctions ◽  
Adrenergic Receptor ◽  
Cardiac Death ◽  
Connexin 43 ◽  
Pressure Overload ◽  
Impulse Conduction ◽  
Cardiac Impulse ◽  
Medical Need

AbstractCardiac arrhythmias are a primary contributor to sudden cardiac death, a major unmet medical need. Because right ventricular (RV) dysfunction increases the risk for sudden cardiac death, we examined responses to RV stress in mice. Among immune cells accumulated in the RV after pressure overload-induced by pulmonary artery banding, interfering with macrophages caused sudden death from severe arrhythmias. We show that cardiac macrophages crucially maintain cardiac impulse conduction by facilitating myocardial intercellular communication through gap junctions. Amphiregulin (AREG) produced by cardiac macrophages is a key mediator that controls connexin 43 phosphorylation and translocation in cardiomyocytes. Deletion of Areg from macrophages led to disorganization of gap junctions and, in turn, lethal arrhythmias during acute stresses, including RV pressure overload and β-adrenergic receptor stimulation. These results suggest that AREG from cardiac resident macrophages is a critical regulator of cardiac impulse conduction and may be a useful therapeutic target for the prevention of sudden death.

Angiotensin II and coronary artery disease, congestive heart failure, and sudden cardiac death

1998 ◽  
Vol 93 (0) ◽  
pp. s101-s108 ◽  
Author(s):  
R. Dietz ◽  
R. von Harsdorf ◽  
M. Gross ◽  
J. Krämer ◽  
D. Gulba ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Angiotensin Ii ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Artery Disease

scholarly journals Association between Angiotensin II Type 1 Receptor Polymorphism and Sudden Cardiac Death in Myocardial Infarction

2013 ◽  
Vol 35 ◽  
pp. 287-293 ◽  
Author(s):  
Peter Kruzliak ◽  
Gabriela Kovacova ◽  
Olga Pechanova ◽  
Stefan Balogh
Keyword(s):  
Myocardial Infarction ◽  
Angiotensin Ii ◽  
Sudden Cardiac Death ◽  
Vascular Remodeling ◽  
Cardiac Death ◽  
Renin Angiotensin System ◽  
Anterior Wall ◽  
Angiotensin System ◽  
Artery Disease

Objective. The renin-angiotensin system is involved in the pathogenesis of coronary artery disease and myocardial infarction (MI). Angiotensin II (Ang II) has many adverse effects such as vasoconstriction and vascular remodeling, and these actions are mediated by the angiotensin II type 1 receptor (AT1R).Patients and Methods. A total of 1376 patients were recruited from January 2010 to April 2012. The study group consisted of 749 patients with ACS (317 females and 432 males) and of 627 healthy controls.Results. The ACS patients demonstrated a lower proportion of AA genotypes and AC genotypes but higher proportions of CC genotypes than the control population. The AT1R CC genotype conferred a 2.76-fold higher risk of MI compared with the genotype AC and AA. In addition, the CC genotype was also associated with a 4.08 times higher risk of left anterior descending artery infarction and a 3.07 times higher risk of anterior wall infarction. We also found that the CC genotype was independently associated with sudden cardiac death.In Summary. This study demonstrated that the AT1R CC genotype is an independent risk factor for ACS incidence, and this genotype is associated with a greater ACS severity and greater risk of sudden cardiac death.

scholarly journals GENE EXPRESSION PATTERN ANALYSIS FOR FORENSIC DIAGNOSIS OF SUDDEN CARDIAC DEATH

2020 ◽  
Vol 4 (9) ◽  
Author(s):  
Saikat Das ◽  
Ritwik Ghosh ◽  
Soumeek Chowdhuri
Keyword(s):  
Gene Expression ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Connexin 43 ◽  
Gene Expression Pattern ◽  
Protein Markers ◽  
Zonula Occludens ◽  
Current Scenario ◽  
Hemoglobin A1 ◽  
Insight Into

Diagnosis of Sudden cardiac death (SCD) is challenging for forensic experts. In the current scenario, genetic analysis is rapidly gaining interest in forensic science. Previous studies are not only limited to using protein markers. In this regard, analysis of mRNA is also a key feature. Analysing mRNA offers insight into the diseases and mechanisms leading to death. It can also be used for forensic diagnostic purposes. This review article takes the help of this methodology to discuss about those mRNA species that can aid in the process of sudden cardiac death (SCD) diagnosis. These are mRNA encoding Heat Shock Protein (HSP), mRNA encoding Hemoglobin A1/2 & B, mRNA encoding Pyruvate Dehydrogenase (PDK4), mRNAs encoding Connexin 43 (Cx43) & Zonula occludens-1 (ZO1), mRNA encoding TNNI3, MYL3, TGFB1, MMP9, VEGFA and mRNA expressing Brain Natriuretic Peptide (BNP).Owing to the difficulty of diagnosing SCD, molecular markers are often developed that can aid in the process. Nowadays, mRNA is showing promising usefulness to supplement the process. Keywords: Sudden Cardiac Death, forensic, gene expression

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