scholarly journals Mitochondrial Oxidation of the Cytoplasmic Reducing Equivalents at the Onset of Oxidant Stress in the Isoproterenol-Induced Rat Myocardial Infarction

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1444
Author(s):  
Olivia Vázquez-Martínez ◽  
Mauricio Díaz-Muñoz ◽  
Fernando López-Barrera ◽  
Rolando Hernández-Muñoz
Keyword(s):  
Myocardial Infarction ◽  
Oxidant Stress ◽  
Myocardial Necrosis ◽  
Atp Synthesis ◽  
Mitochondrial Activity ◽  
Cardiac Damage ◽  
Relevant Role ◽  
Functional Consequences ◽  
Malate Aspartate Shuttle ◽  
Reducing Equivalents

We have developed and characterized a model of isoproterenol (ISO)-induced myocardial necrosis, identifying three stages of cardiac damage: a pre-infarction (0–12 h), infarction (24 h), and post-infarction period (48–96 h). Using this model, we have previously found alterations in calcium homeostasis and their relationship with oxidant stress in mitochondria, which showed deficient oxygen consumption and coupled ATP synthesis. Therefore, the present study was aimed at assessing the mitochondrial ability to transport and oxidize cytoplasmic reducing equivalents (NADH), correlating the kinetic parameters of the malate-aspartate shuttle, oxidant stress, and mitochondrial functionality. Our results showed only discreet effects during the cardiotoxic ISO action on the endogenous malate-aspartate shuttle activity, suggesting that endogenous mitochondrial NADH oxidation capacity (Nohl dehydrogenase) was not affected by the cellular stress. On the contrary, the reconstituted system showed significant enhancement in maximal capacity of the malate-aspartate shuttle activity only at later times (post-infarction period), probably as a compensatory part of cardiomyocytes’ response to the metabolic and functional consequences of the infarcted tissue. Therefore, these findings support the notion that heart damage associated with myocardial infarction suffers a set of sequential biochemical and metabolic modifications within cardiomyocytes, where mitochondrial activity, controlling the redox state, could play a relevant role.

scholarly journals Photobiomodulation Regulation as One Promising Therapeutic Approach for Myocardial Infarction

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Xinlu Gao ◽  
Wenwen Zhang ◽  
Fan Yang ◽  
Wenya Ma ◽  
Benzhi Cai
Keyword(s):  
Myocardial Infarction ◽  
Molecular Mechanisms ◽  
Contractile Function ◽  
Heart Function ◽  
Myocardial Necrosis ◽  
Atp Synthesis ◽  
Source Power ◽  
Positive Effects ◽  
Promising Therapeutic Approach ◽  
Improve Heart Function

Myocardial infarction refers to myocardial necrosis caused by acute or persistent coronary ischemia and hypoxia. It is considered to be one of the significant crises threatening human health in the world. Following myocardial infarction, collagen gradually replaces the original tissue due to the loss of many cardiomyocytes, myocardial contractile function decreases, and myocardial fibrosis eventually leads to heart failure. Phototherapy is a new treatment which has shown superior efficacy on the nerve, skeletal muscle, skin, and other tissues. Likewise, there is growing evidence that phototherapy also has many positive effects on the heart. Therefore, this article introduces the progress of research on phototherapy as a new therapeutic strategy in the treatment of myocardial infarction. The wavelength of photobiomodulation in the treatment of myocardial infarction is specific, and the influence of light source power and light duration on the tissue presents a bell-shaped distribution. Under these conditions, phototherapy can promote ATP synthesis and angiogenesis, inhibit the inflammatory response, improve heart function, reduce infarct size, and protect myocardium. In addition, we summarized the molecular mechanisms of phototherapy. According to the location of photoreceptors, they can be divided into mitochondrial and nonmitochondrial parts.

scholarly journals Therapies Targeted at Non-Coding RNAs in Prevention and Limitation of Myocardial Infarction and Subsequent Cardiac Remodeling—Current Experience and Perspectives

2021 ◽  
Vol 22 (11) ◽  
pp. 5718
Author(s):  
Michal Kowara ◽  
Sonia Borodzicz-Jazdzyk ◽  
Karolina Rybak ◽  
Maciej Kubik ◽  
Agnieszka Cudnoch-Jedrzejewska
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Cardiac Remodeling ◽  
Therapeutic Option ◽  
Circular Rna ◽  
Plaque Progression ◽  
Cardiac Damage ◽  
Non Coding Rna ◽  
Causes Of Mortality ◽  
Long Non Coding Rna

Myocardial infarction is one of the major causes of mortality worldwide and is a main cause of heart failure. This disease appears as a final point of atherosclerotic plaque progression, destabilization, and rupture. As a consequence of cardiomyocytes death during the infarction, the heart undergoes unfavorable cardiac remodeling, which results in its failure. Therefore, therapies aimed to limit the processes of atherosclerotic plaque progression, cardiac damage during the infarction, and subsequent remodeling are urgently warranted. A hopeful therapeutic option for the future medicine is targeting and regulating non-coding RNA (ncRNA), like microRNA, circular RNA (circRNA), or long non-coding RNA (lncRNA). In this review, the approaches targeted at ncRNAs participating in the aforementioned pathophysiological processes involved in myocardial infarction and their outcomes in preclinical studies have been concisely presented.

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.

Mineralocorticoid Receptor Activation by Aldosterone or Corticosterone Induces Hypertension, Myocardial Infarction and Proteinuria

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 723-723
Author(s):  
Qing-Feng Tao ◽  
Diego Martinez vasquez ◽  
Ricardo Rocha ◽  
Gordon H Williams ◽  
Gail K Adler
Keyword(s):  
Myocardial Infarction ◽  
Drinking Water ◽  
Mineralocorticoid Receptor ◽  
Critical Role ◽  
Weight Ratio ◽  
Myocardial Necrosis ◽  
Receptor Activation ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

P165 Aldosterone through its interaction with the mineralocorticoid receptor (MR) plays a critical role in the development of hypertension and cardiovascular injury (CVI). Normally, MR is protected by 11β-hydroxysteroid dehydrogenase (11β-HSD) which inactivates glucocorticoids preventing their binding to MR. We hypothesis that if activation of MR by either aldosterone or glucocorticoids induces hypertension and CVI, then the inhibition of 11β-HSD with glycyrrhizin (GA), a natural inhibitor of 11β-HSD, should induce damage similar to that observed with aldosterone. Sprague-Dawley rats were uninephrectomized, and treated for 4 weeks with 1% NaCl (in drinking water) for the control group, 1% NaCl + aldosterone infusion (0.75 μg/h), or 1% NaCl + GA (3.5 g/l in drinking water). After 4 weeks, aldosterone and GA caused significant increases in blood pressure compared to control rats ([mean ± SEM] 211± 9, 205 ± 12, 120 ± 9 mmHg, respectively, p<0.001). Both aldosterone- and GA-treated rats had a significant increase in proteinuria (152.2 ± 8.7 and 107.7 ± 19.5 mg/d, respectively) versus controls (51.2 ± 9.5 mg/d). There was a significant increase (p<0.001) in heart to body weight ratio in the rats treated with aldosterone or GA compared with control (3.92 ± 0.10, 3.98 ± 0.88, and 3.24 ± 0.92 mg/g, respectively). Hearts of GA and aldosterone treated rats showed similar histological changes consisting of biventricular myocardial necrosis and fibrinoid necrosis of small coronary arteries and arterioles. These data suggests that in rodents activation of MR by either aldosterone or corticosterone leads to severe hypertension, vascular injury, proteinuria and myocardial infarction. Thus, 11β-HSD plays an important role in protecting the organism from injury.

scholarly journals Case Report: Identification of a Novel Variant (m.8909T>C) of Human Mitochondrial ATP6 Gene and Its Functional Consequences on Yeast ATP Synthase

Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 215
Author(s):  
Qiuju Ding ◽  
Róża Kucharczyk ◽  
Weiwei Zhao ◽  
Alain Dautant ◽  
Shutian Xu ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Atp Synthase ◽  
Atp Synthesis ◽  
Single Individual ◽  
Loss Of Function ◽  
Mtdna Mutations ◽  
Atp6 Gene ◽  
Novel Variant ◽  
Functional Consequences ◽  
Mtdna Variants

With the advent of next generation sequencing, the list of mitochondrial DNA (mtDNA) mutations identified in patients rapidly and continuously expands. They are frequently found in a limited number of cases, sometimes a single individual (as with the case herein reported) and in heterogeneous genetic backgrounds (heteroplasmy), which makes it difficult to conclude about their pathogenicity and functional consequences. As an organism amenable to mitochondrial DNA manipulation, able to survive by fermentation to loss-of-function mtDNA mutations, and where heteroplasmy is unstable, Saccharomyces cerevisiae is an excellent model for investigating novel human mtDNA variants, in isolation and in a controlled genetic context. We herein report the identification of a novel variant in mitochondrial ATP6 gene, m.8909T>C. It was found in combination with the well-known pathogenic m.3243A>G mutation in mt-tRNALeu. We show that an equivalent of the m.8909T>C mutation compromises yeast adenosine tri-phosphate (ATP) synthase assembly/stability and reduces the rate of mitochondrial ATP synthesis by 20–30% compared to wild type yeast. Other previously reported ATP6 mutations with a well-established pathogenicity (like m.8993T>C and m.9176T>C) were shown to have similar effects on yeast ATP synthase. It can be inferred that alone the m.8909T>C variant has the potential to compromise human health.

scholarly journals Troponin T and Histological Characteristics of Rat Myocardial Infarction Induced by Isoproterenol

2007 ◽  
Vol 7 (3) ◽  
pp. 212-217 ◽  
Author(s):  
Sabaheta Hasić ◽  
Radivoj Jadrić ◽  
Emina Kiseljaković ◽  
Zakira Mornjaković ◽  
Mira Winterhalter-Jadrić
Keyword(s):  
Myocardial Infarction ◽  
Troponin T ◽  
Myocardial Necrosis ◽  
Control Group ◽  
High Dose ◽  
Male Adult ◽  
Histological Changes ◽  
Significant Difference ◽  
Intraperitoneal Dose ◽  
Histological Characteristics

In our investigation, we used short-time model of myocardial infarction of rats induced by high dose of isoproterenol (ISP). We investigated cardiac troponin T blood level (cTnT) and histological characteristics of rat myocardium. ISP, single, intraperitoneal dose 250 mg/kg was given to male, adult, Wistar rats (n=12). Rats were distributed depending on their body weight in subgroups: ISP I (BW 260-280g) and ISP II (BW 250-400g). Control group (n=9) was treated with intraperitoneal dose of 0,95% NaCl. Cardiac TnT was measured by electrochemiluminiscence (ECLA) sandwich immunoassay in rat serum 4 hours after ISP application. Rats’ hearts were dissected and examined by qualitative histological method (HE). Statistical significance was set at 0,05. There was significant difference in cTnT of ISP II (p=0,0001) vs. control and ISP I (p<0,05) vs. control. Significant difference was beetween ISP I and ISP II subgroups (p<0.001). The accent of histological changes of myocardium was on nuclei of cell. Cells showed acydophilic changes and nuclei disappearance as signs of coagulative necrosis development. Extensivity of histological changes were different beetween ISP I and ISP II subgroup. Used dose of ISP induced development of myocardial necrosis in rats. Suben-docardial portion of myocardium was more vulnerability than subepicardial portion. Rats of ISP II had more extensive histological changes than these in ISP I. Administered doses of ISP enabled cTnT utilization as a marker of myocardial necrosis.

scholarly journals ACUTE MYOCARDIAL INFARCTION SPECIFICS IN PATIENTS WITH CHRONIC TONSILLITIS

2014 ◽  
Vol 13 (1) ◽  
pp. 22-26
Author(s):  
Kh. R. Dzhukaeva ◽  
Yu. G. Schwartz
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Qt Interval ◽  
Clinical Course ◽  
Myocardial Necrosis ◽  
Chronic Tonsillitis ◽  
Ecg Monitoring ◽  
Glucose Levels ◽  
Qt Interval Dispersion ◽  
Interval Dispersion

Aim. To investigate the clinical specifics of acute myocardial infarction(AMI) in patients with chronic tonsillitis.Material and methods. The study included 70 patients at early AMI stages (Days 1–2). The following parameters were analysed: anthropometry, blood biochemistry, myocardial necrosis markers, QT interval dispersion, echocardiography and Holter ECG monitoring parameters, and a confirmed medical diagnosis of chronic tonsillitis in medical history.Results. In 31 patients with confirmed chronic tonsillitis, higher body mass index values, a significantly higher incidence of acute heart failure (19,4%; p<0,05) and anterior AMI (70%), higher glucose levels at admission (7,58±0,62 mmol/l), and a higher end-diastolic size of right ventriculum (3,04±0,19 cm vs. 2,66±0,05 cm) were observed. Mean daytime and peak nighttime heart rate values were higher than in other patients.Conclusion. Patients with confirmed chronic tonsillitis were characterised by a more severe clinical course of AMI. There is some evidence that chronic tonsillitis is also associated with metabolic syndrome.

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