scholarly journals NETosis as a Pathogenic Factor for Heart Failure

2021 ◽  
Vol 2021 ◽  
pp. 1-24
Author(s):  
Shuang Ling ◽  
Jin-Wen Xu
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Bacterial Infections ◽  
Defense Mechanism ◽  
Tissue Injury ◽  
Heart Diseases ◽  
Immune Defense ◽  
Low Grade ◽  
Aseptic Inflammation

Heart failure threatens the lives of patients and reduces their quality of life. Heart failure, especially heart failure with preserved ejection fraction, is closely related to systemic and local cardiac persistent chronic low-grade aseptic inflammation, microvascular damage characterized by endothelial dysfunction, oxidative stress, myocardial remodeling, and fibrosis. However, the initiation and development of persistent chronic low-grade aseptic inflammation is unexplored. Oxidative stress-mediated neutrophil extracellular traps (NETs) are the main immune defense mechanism against external bacterial infections. Furthermore, NETs play important roles in noninfectious diseases. After the onset of myocardial infarction, atrial fibrillation, or myocarditis, neutrophils infiltrate the damaged tissue and aggravate inflammation. In tissue injury, damage-related molecular patterns (DAMPs) may induce pattern recognition receptors (PRRs) to cause NETs, but whether NETs are directly involved in the pathogenesis and development of heart failure and the mechanism is still unclear. In this review, we analyzed the markers of heart failure and heart failure-related diseases and comorbidities, such as mitochondrial DNA, high mobility box group box 1, fibronectin extra domain A, and galectin-3, to explore their role in inducing NETs and to investigate the mechanism of PRRs, such as Toll-like receptors, receptor for advanced glycation end products, cGAS-STING, and C-X-C motif chemokine receptor 2, in activating NETosis. Furthermore, we discussed oxidative stress, especially the possibility that imbalance of thiol redox and MPO-derived HOCl promotes the production of 2-chlorofatty acid and induces NETosis, and analyzed the possibility of NETs triggering coronary microvascular thrombosis. In some heart diseases, the deletion or blocking of neutrophil-specific myeloperoxidase and peptidylarginine deiminase 4 has shown effectiveness. According to the results of current pharmacological studies, MPO and PAD4 inhibitors are effective at least for myocardial infarction, atherosclerosis, and certain autoimmune diseases, whose deterioration can lead to heart failure. This is essential for understanding NETosis as a therapeutic factor of heart failure and the related new pathophysiology and therapeutics of heart failure.

scholarly journals Oxidative Stress-Responsive MicroRNAs in Heart Injury

2020 ◽  
Vol 21 (1) ◽  
pp. 358 ◽  
Author(s):  
Branislav Kura ◽  
Barbara Szeiffova Bacova ◽  
Barbora Kalocayova ◽  
Matus Sykora ◽  
Jan Slezak
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ischemia Reperfusion Injury ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Related Factor ◽  
Nuclear Factor ◽  
Stress Oxidative ◽  
Living Organisms

Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and heart transplantation), and heart failure. As a result of oxidative stress action, apoptosis, hypertrophy, and fibrosis may occur. MicroRNAs (miRNAs) represent important endogenous nucleotides that regulate many biological processes, including those involved in heart damage caused by oxidative stress. Oxidative stress can alter the expression level of many miRNAs. These changes in miRNA expression occur mainly via modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuins, calcineurin/nuclear factor of activated T cell (NFAT), or nuclear factor kappa B (NF-κB) pathways. Up until now, several circulating miRNAs have been reported to be potential biomarkers of ROS-related cardiac diseases, including myocardial infarction, hypertrophy, ischemia/reperfusion, and heart failure, such as miRNA-499, miRNA-199, miRNA-21, miRNA-144, miRNA-208a, miRNA-34a, etc. On the other hand, a lot of studies are aimed at using miRNAs for therapeutic purposes. This review points to the need for studying the role of redox-sensitive miRNAs, to identify more effective biomarkers and develop better therapeutic targets for oxidative-stress-related heart diseases.

Role of oxidative stress in left ventricular remodeling and heart failure after myocardial infarction

1999 ◽  
Vol 5 (3) ◽  
pp. 79
Author(s):  
Shintaro Kinugawa ◽  
Hiroyuki Tsutsui ◽  
Tomomi Ide ◽  
Hideo Ustumi ◽  
Nobuhiro Suematsu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular

Abstract 814: Atorvastatin Attenuates Oxidative Stress And Improves Neuronal Nitric Oxide Synthase In The Brain Stem Of Heart Failure Mice

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Joseph Francis ◽  
Li Yu ◽  
Anuradha Guggilam ◽  
Srinivas Sriramula ◽  
Irving H Zucker
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Brain Stem ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Neuronal Nos ◽  
The Brain

3-Hydroxyl-3-methylglutaryl coenzyme A reductase inhibitors (statins) have been shown to reduce the incidence of myocardial infarction independent of their lipid-lowering effects. Nitric oxide (NO) in the central nervous system contributes to cardiovascular regulatory mechanisms. Imbalance between nitric oxide (NO) and superoxide anion (O 2 . − ) in the brain may contribute to enhanced sympathetic drive in heart failure (HF). This study was done to determine whether treatment with atorvastatin (ATS) ameliorates the imbalance between NO and O 2 . − production in the brain stem and contributes to improvement of left ventricular (LV) function. Methods and Results: Myocardial infarction (MI) was induced by ligation of the left coronary artery or sham surgery. Subsequently, mice were treated with ATS (10 μg/kg) (MI + ATS), or vehicle (MI + V). After 5 weeks, echocardiography revealed left ventricular dilatation in MI mice. Realtime RT-PCR indicated an increase in the mRNA expression of the LV hypertrophy markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). Neuronal NOS (nNOS) and endothelial NOS (eNOS) mRNA expression were significantly reduced, while that of NAD(P)H oxidase subunit (gp91phox) expression was elevated in the brain stem of MI mice. Compared with sham-operated mice, ATS-treated mice showed reduced cardiac dilatation, decreased ANP and BNP in the LV. ATS also reduced gp91phox expression and increased nNOS mRNA expression in the brain stem, while no changes in eNOS and iNOS were observed. Conclusion: These findings suggest that ATS reduces oxidative stress and increases neuronal NOS in the brain stem, and improves left ventricular function in heart failure.

scholarly journals Mortality Sensitivity of Cardiovascular, Cerebrovascular, and Respiratory Diseases to Warm Season Climate in Japanese Cities

Atmosphere ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1546
Author(s):  
Yukitaka Ohashi ◽  
Akari Miyata ◽  
Tomohiko Ihara
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Respiratory Diseases ◽  
Heart Diseases ◽  
Warm Season ◽  
Respiratory Mortality ◽  
Ischemic Heart Diseases ◽  
Mean Temperature ◽  
Risk Ratios

We investigated decadal (2010–2019) cardiovascular, cerebrovascular, and respiratory mortality sensitivity to annual warm temperatures in major Japanese cities: Sapporo, Tokyo (23 wards), and Osaka. The summer mortalities (June–August) increased with the monthly mean temperature for acute myocardial infarction, other acute ischemic heart diseases, cerebral infarction, and pneumonia in the three cities. Monthly mean temperatures were an indicator of these disease mortalities in Japan. However, similar responses were not found for cardiac arrhythmia and heart failure (excluding Sapporo), subarachnoid hemorrhage, and intracerebral hemorrhage. The decadal sensitivities and risk ratios between the maximum and minimum monthly mean temperatures were calculated using a linear regression model. In Sapporo, Tokyo, and Osaka, for example, the analyses of acute myocardial infarction showed summer positive responses of 0.19–0.25, 0.13–0.18, and 0.12–0.30, respectively, as the mortality rate (per 100,000 population) per 1 °C of monthly mean temperature, which estimated increased risks (between the coolest and hottest months) of 37–65% in Sapporo, 31–42% in Tokyo, and 35–39% in Osaka.

scholarly journals Macrophage Activities in Myocardial Infarction and Heart Failure

2020 ◽  
Vol 2020 ◽  
pp. 1-16 ◽  
Author(s):  
Sophia Esi Duncan ◽  
Shan Gao ◽  
Michael Sarhene ◽  
Joel Wake Coffie ◽  
Deng Linhua ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Left Ventricular Systolic Dysfunction ◽  
Heart Diseases ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Hibernating Myocardium ◽  
Clear Understanding ◽  
Myocardial Repair

Heart diseases remain the major cause of death worldwide. Advances in pharmacological and biomedical management have resulted in an increasing proportion of patients surviving acute heart failure (HF). However, many survivors of HF in the early stages end up increasing the disease to chronic HF (CHF). HF is an established frequent complication of myocardial infarction (MI), and numerous influences including persistent myocardial ischemia, shocked myocardium, ventricular remodeling, infarct size, and mechanical impairments, as well as hibernating myocardium trigger the development of left ventricular systolic dysfunction following MI. Macrophage population is active in inflammatory process, yet the clear understanding of the causative roles for these macrophage cells in HF development and progression is actually incomplete. Long ago, it was thought that macrophages are of importance in the heart after MI. Also, though inflammation is as a result of adverse HF in patients, but despite the fact that broad immunosuppression therapeutic target has been used in various clinical trials, no positive results have showed up, but rather, the focus on proinflammatory cytokines has proved more benefits in patients with HF. Therefore, in this review, we discuss the recent findings and new development about macrophage activations in HF, its role in the healthy heart, and some therapeutic targets for myocardial repair. We have a strong believe that there is a need to give maximum attention to cardiac resident macrophages due to the fact that they perform various tasks in wound healing, self-renewal of the heart, and tissue remodeling. Currently, it has been discovered that the study of macrophages goes far beyond its phagocytotic roles. If researchers in future confirm that macrophages play a vital role in the heart, they can be therapeutically targeted for cardiac healing.

scholarly journals Cytochrome c oxidase III as a mechanism for apoptosis in heart failure following myocardial infarction

2009 ◽  
Vol 297 (4) ◽  
pp. C928-C934 ◽  
Author(s):  
Changgong Wu ◽  
Lin Yan ◽  
Christophe Depre ◽  
Sunil K. Dhar ◽  
You-Tang Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Cytochrome C ◽  
Protein Expression ◽  
Cell Viability ◽  
Cytochrome C Oxidase ◽  
Mitochondrial Gene

Cytochrome c oxidase (COX) is composed of 13 subunits, of which COX I, II, and III are encoded by a mitochondrial gene. COX I and II function as the main catalytic components, but the function of COX III is unclear. Because myocardial ischemia affects mitochondrial oxidative metabolism, we hypothesized that COX activity and expression would be affected during postischemic cardiomyopathy. This hypothesis was tested in a monkey model following myocardial infarction (MI) and subsequent pacing-induced heart failure (HF). In this model, COX I protein expression was decreased threefold after MI and fourfold after HF ( P < 0.05 vs. sham), whereas COX II expression remained unchanged. COX III protein expression increased 5-fold after MI and further increased 10-fold after HF compared with sham ( P < 0.05 vs. sham). The physiological impact of COX III regulation was examined in vitro. Overexpression of COX III in mitochondria of HL-1 cells resulted in an 80% decrease in COX I, 60% decrease in global COX activity, 60% decrease in cell viability, and threefold increase in apoptosis ( P < 0.05). Oxidative stress induced by H2O2 significantly ( P < 0.05) increased COX III expression. H2O2 decreased cell viability by 47 ± 3% upon overexpression of COX III, but only by 12 ± 5% in control conditions ( P < 0.05). We conclude that ischemic stress in vivo and oxidative stress in vitro lead to upregulation of COX III, followed by downregulation of COX I expression, impaired COX oxidative activity, and increased apoptosis. Therefore, upregulation of COX III may contribute to the increased susceptibility to apoptosis following MI and subsequent HF.

scholarly journals The influence of the autonomic nervous system in the development of chronic heart failure in patients with chronic brain ischemia combined with myocardial infarction

2018 ◽  
pp. 37-40
Author(s):  
N. O. Kravchuk
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Chronic Heart Failure ◽  
Heart Diseases ◽  
Clinical Syndrome ◽  
Chronic Cerebral Ischemia ◽  
Course Of Disease ◽  
Number Of Patients ◽  
Chronic Brain Ischemia

Heart failure - severe, common clinical syndrome that is the result of many heart diseases is progressive, significantly reduces the life expectancy of patients and impairs its quality. Leading nosological forms the structure of coronary heart disease for many years, is a myocardial infarction. Growing proportion of elderly in most populations, increased survival after acute myocardial infarction (AMI) resulted in a significant increase in the number of patients with chronic heart failure (CHF). Increased tone of the sympathetic division precedes the development of chronic cerebral ischemia and, therefore, may complicate the course of disease in the presence of chronic heart failure.

scholarly journals Cardioprotective role of myocardial endothelial nitric oxide synthase and serum nitric oxide induced by hexarelin in rats with myocardial infarction-induced heart failure

2021 ◽  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Left Ventricular ◽  
Nitric Oxide Level ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background: Growth hormone-releasing peptides (GHRP) have been reported to possess cardioprotective properties; nonetheless, their mechanisms of action are still not very clear. Objectives: Some studies have suggested that modulation of endothelial nitric oxide synthase (eNOS) and the upregulation of nitric oxide (NO) are cardioprotective. Therefore, the present study strived to test the hypothesis that a potent GHRP analog (hexarelin) could increase serum nitric oxide level and regulate myocardial eNOS to alleviate the development of heart failure. Methods: Myocardial infarction-induced heart failure in rats was established by permanent coronary artery ligation. The sham group, control group, and heart failure group all received normal saline (100 µg/kg; SC BID; 30days), while the rats in the hexarelin treatment group were treated with hexarelin (100 µg/kg, SC BID, 30 days). The rats were tested for myocardial apoptosis, oxidative stress, left ventricular function, various molecular analyses, as well as pathological and structural myocardial changes. Results: Hexarelin treatment improved contractile function and attenuated myocardial histopathological damages, oxidative stress, fibrosis, as well as apoptosis. All these were accompanied by the upregulation of myocardial eNOS and an increase in serum NO concentration. Conclusion: As evidenced by the obtained results, the anti-cardiac failure capacity of hexarelinin in a rat model is mediated by an increase in serum nitric oxide level and the up-modulation of myocardial eNOS; therefore, they can be considered therapeutic targets against heart failure.

scholarly journals The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism

2020 ◽  
Author(s):  
Qi Chen ◽  
Dini Zhang ◽  
Yunhui Bi ◽  
Weiwei Zhang ◽  
Yuhan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Myocardial Cell ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Cardiac Functions ◽  
Tgf Β1

Abstract Background : Heart failure (HF) is one of the most common causes of cardiovascular diseases in the world. Currently, the drugs used to treat HF in the clinic may cause serious side effects. Liguzinediol, 2, 5-dimethyl-3, 6-dimethyl-pyrazine, is a compound synthesized after the structural modification of ligustrazine (one active ingredient of Szechwan Lovage Rhizome ). We aimed to observe the effects of liguzinediol on preventing HF and explore the related mechanisms. Methods : The ligation of left anterior descending coronary artery was operated to established the myocardial infarction (MI) model in Sprague–Dawley rats. Cardiac functions were recorded by echocardiography and hemodynamics. The changes in the Renin-Angiotensin-Aldosterone System (RAAS), inflammation, and oxidative stress were detected by radioimmunoassay and Elisa kits. Western blot and real-time PCR were applied to determine the expressions of the TGF-β1/Smads pathway. Results : Firstly, liguzinediol enhanced the systolic and diastolic functions of the heart in MI rats. Liguzinediol improved ventricular remodeling by reducing myocardial cell necrosis, as well as reducing collagen deposition and myocardial fibrosis. Then, liguzinediol suppressed the activation of RAAS, inhibited the synthesis of pro-inflammation factors, and reduced oxidative stress. In the end, liguzinediol also down-regulated the expressions of the TGF-β1/Smads pathway. Conclusions : Liguzinediol could alleviate HF caused by MI in rats, and the protective effect was associated with the regulation of the TGF-β1/Smads pathway.

Oxidative stress and hemorheology in patients myocardial infarction with type 2 diabetes

2015 ◽  
Vol 9 (4) ◽  
pp. 0-0 ◽  
Author(s):  
Гончарова ◽  
E. Goncharova ◽  
Ойноткинова ◽  
O. Oynotkinova ◽  
Корниенко ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Lipid Peroxidation ◽  
Acute Heart Failure ◽  
Blood Cells ◽  
Diabetes Type 2 ◽  
Diabetes Type

This paper highlights the influence of the intensity of the oxidative stress on hemorheology parameters in complicated and uncomplicated acute myocardial infarction in patients with diabetes type 2. The study was performed by analyzing the results of examination and treatment of 66 patients, men aged 65,6 ± 5,8 years old, suffering from coronary heart disease with clinical manifestations of acute myocardial infarction and concomitant diabetes type 2. Depending on the presence of acute heart failure patients were divided into 2 groups. 1st group consisted of 34 patients with myocardial infarction without complications, Group 2 - 32 patients who have myocardial infarction complicated by acute heart failure (II-III class classification T.Killip). Condition pro- and antioxidant systems were evaluated for 3 days by determining in the blood of patients diene conjugates, malonic dialdehyde, α-tocopherol, ceruloplasmin, calculated coefficient of oxidative stress. The rheological properties blood evaluated by the blood coagulation time, the hematocrit, amount the fibrinogen in the blood, and blood plasma viscosity, red blood cells deformability index, the aggregation of red blood cells and thrombocytes. The values obtained were compared with data from 32 healthy donors. It is revealed that the development of congestive heart failure in acute myocardial infarction in patients with diabetes type 2 is accompanied by activation of lipid peroxidation (LPO) by maintaining a high level of primary lipid peroxidation products. Insufficient activity of antioxidant defense can limit oxidative processes, and leads to their further growth. The damaging effect of lipid peroxidation in the cell membranes is reflected in violation of aggregation and blood viscosity indexes.

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