scholarly journals Protective Effects of Estrogen on Cardiovascular Disease Mediated by Oxidative Stress

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Du Xiang ◽  
Yang Liu ◽  
Shujun Zhou ◽  
Encheng Zhou ◽  
Yanfeng Wang
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiovascular Disease ◽  
Estrogen Receptor ◽  
Cardiovascular System ◽  
Myocardial Dysfunction ◽  
Premenopausal Women ◽  
Protective Effects ◽  
Epidemiological Investigation ◽  
Menopausal Women

Perimenopause is an important stage of female senescence. Epidemiological investigation has shown that the incidence of cardiovascular disease in premenopausal women is lower than that in men, and the incidence of cardiovascular disease in postmenopausal women is significantly higher than that in men. This phenomenon reveals that estrogen has a definite protective effect on the cardiovascular system. In the cardiovascular system, oxidative stress is considered important in the pathogenesis of atherosclerosis, myocardial dysfunction, cardiac hypertrophy, heart failure, and myocardial ischemia. From the perspective of oxidative stress, estrogen plays a regulatory role in the cardiovascular system through the estrogen receptor, providing strategies for the treatment of menopausal women with cardiovascular diseases.

Accumulation of 5-oxoproline in myocardial dysfunction and the protective effects of OPLAH

2017 ◽  
Vol 9 (415) ◽  
pp. eaam8574 ◽  
Author(s):  
Atze van der Pol ◽  
Andres Gil ◽  
Herman H. W. Silljé ◽  
Jasper Tromp ◽  
Ekaterina S. Ovchinnikova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Myocardial Dysfunction ◽  
Cardiac Injury ◽  
Transcriptional Analysis ◽  
Protective Effects ◽  
Elevated Plasma ◽  
Gene Profile ◽  
Adult Mice ◽  
And Oxidative Stress

In response to heart failure (HF), the heart reacts by repressing adult genes and expressing fetal genes, thereby returning to a more fetal-like gene profile. To identify genes involved in this process, we carried out transcriptional analysis on murine hearts at different stages of development and on hearts from adult mice with HF. Our screen identified Oplah, encoding for 5-oxoprolinase, a member of the γ-glutamyl cycle that functions by scavenging 5-oxoproline. OPLAH depletion occurred as a result of cardiac injury, leading to elevated 5-oxoproline and oxidative stress, whereas OPLAH overexpression improved cardiac function after ischemic injury. In HF patients, we observed elevated plasma 5-oxoproline, which was associated with a worse clinical outcome. Understanding and modulating fetal-like genes in the failing heart may lead to potential diagnostic, prognostic, and therapeutic options in HF.

scholarly journals The Role of Estrogen Receptors in Cardiovascular Disease

2020 ◽  
Vol 21 (12) ◽  
pp. 4314 ◽  
Author(s):  
Laila Aryan ◽  
David Younessi ◽  
Michael Zargari ◽  
Somanshu Banerjee ◽  
Jacqueline Agopian ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Estrogen Receptor ◽  
Ejection Fraction ◽  
Estrogen Receptors ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Vascular Pathology ◽  
Reduced Ejection Fraction

Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially serve as a cardioprotective agent. The effects of estrogen on cardiovascular function are mediated by nuclear and membrane estrogen receptors (ERs), including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled ER (GPR30 or GPER). Receptor binding in turn confers pleiotropic effects through both genomic and non-genomic signaling to maintain cardiovascular homeostasis. Each ER has been implicated in multiple pre-clinical cardiovascular disease models. This review will discuss current reports on the underlying molecular mechanisms of the ERs in regulating vascular pathology, with a special emphasis on hypertension, pulmonary hypertension, and atherosclerosis, as well as in regulating cardiac pathology, with a particular emphasis on ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction.

scholarly journals Magnesium, Oxidative Stress, Inflammation, and Cardiovascular Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 907 ◽  
Author(s):  
Man Liu ◽  
Samuel C. Dudley
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Heart Failure ◽  
Cardiovascular Disease ◽  
Clinical Trials ◽  
Cardiovascular Diseases ◽  
Serum Magnesium ◽  
Mg Deficiency ◽  
All Cause Mortality ◽  
Low Serum

Hypomagnesemia is commonly observed in heart failure, diabetes mellitus, hypertension, and cardiovascular diseases. Low serum magnesium (Mg) is a predictor for cardiovascular and all-cause mortality and treating Mg deficiency may help prevent cardiovascular disease. In this review, we discuss the possible mechanisms by which Mg deficiency plays detrimental roles in cardiovascular diseases and review the results of clinical trials of Mg supplementation for heart failure, arrhythmias and other cardiovascular diseases.

scholarly journals Nicotinamide riboside promotes autolysosome clearance in preventing doxorubicin-induced cardiotoxicity

2019 ◽  
Vol 133 (13) ◽  
pp. 1505-1521 ◽  
Author(s):  
Dong Zheng ◽  
Yi Zhang ◽  
Ming Zheng ◽  
Ting Cao ◽  
Grace Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanism ◽  
Myocardial Dysfunction ◽  
Cardiac Injury ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Nicotinamide Riboside ◽  
And Oxidative Stress ◽  
Cultured Cardiomyocytes ◽  
Lysosomal Acidification

Abstract Doxorubicin (DOX) is widely used as a first-line chemotherapeutic drug for various malignancies. However, DOX causes severe cardiotoxicity, which limits its clinical uses. Oxidative stress is one of major contributors to DOX-induced cardiotoxicity. While autophagic flux serves as an important defense mechanism against oxidative stress in cardiomyocytes, recent studies have demonstrated that DOX induces the blockage of autophagic flux, which contributes to DOX cardiotoxicity. The present study investigated whether nicotinamide riboside (NR), a precursor of nicotinamide adenine dinucleotide (NAD)+, prevents DOX cardiotoxicity by improving autophagic flux. We report that administration of NR elevated NAD+ levels, and reduced cardiac injury and myocardial dysfunction in DOX-injected mice. These protective effects of NR were recapitulated in cultured cardiomyocytes upon DOX treatment. Mechanistically, NR prevented the blockage of autophagic flux, accumulation of autolysosomes, and oxidative stress in DOX-treated cardiomyocytes, the effects of which were associated with restoration of lysosomal acidification. Furthermore, inhibition of lysosomal acidification or SIRT1 abrogated these protective effects of NR during DOX-induced cardiotoxicity. Collectively, our study shows that NR enhances autolysosome clearance via the NAD+/SIRT1 signaling, thereby preventing DOX-triggered cardiotoxicity.

scholarly journals Butein Inhibits Oxidative Stress Injury in Rats with Chronic Heart Failure via ERK/Nrf2 Signaling

2022 ◽  
Vol 2022 ◽  
pp. 1-10
Author(s):  
Peng Liu ◽  
Quanli Pan
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Stress Injury ◽  
Oxidative Stress Injury

Background. Chronic heart failure (CHF) is a serious heart disease resulting from cardiac dysfunction. Oxidative stress is an important factor in aging and disease. Butein, however, has antioxidant properties. To determine the effect of butein on oxidative stress injury in rats, a CHF rat model was established. Methods. The CHF rat model was induced by abdominal aortic coarctation (AAC). Rats in CHF+butein and sham+butein group were given 100 mg/kg butein via gavage every day to detect the effect of butein on oxidative stress injury and myocardial dysfunction. The cardiac structural and functional parameters, including the left ventricular end-systolic dimension (LVESD), the left ventricular end-diastolic dimension (LVEDD), the left ventricular ejection fraction (LVEF), and the left ventricular fractional shortening (LVFS), were measured. Oxidative stress was measured through the production of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA). Cardiac injury markers like creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) were evaluated. Hematoxylin and eosin (H&E) staining was used to observe the myocardial cell morphology. The effect of butein on the extracellular signal-regulated kinase (ERK)/nuclear factor-E2 p45-related factor (Nrf2) signaling was confirmed by Western blot analysis. Results. Butein had a significant effect on CHF in animal models. In detail, butein inhibited oxidative stress, relieved cardiac injury, and alleviated myocardial dysfunction. Importantly, butein activated the ERK1/2 pathway, which contributed to Nrf2 activation and subsequent heme oxygenase-1 (HO-1) and glutathione cysteine ligase regulatory subunit (GCLC) induction. Conclusions. In this study, butein inhibits oxidative stress injury in CHF rat model via ERK/Nrf2 signaling pathway.

scholarly journals Protective Effects of Myrtus communis Linn Fruit and Leaf Extracts on Isoproterenol-Induced Heart Failure in Rat

2021 ◽  
Author(s):  
Nahid Aboutaleb ◽  
Fataneh Hashem-Dabaghian ◽  
Azinmehr Elahian Boroujeni ◽  
Asie Shojaii
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Cardiac Fibrosis ◽  
Experimental Period ◽  
Stress Factors ◽  
Control Group ◽  
Alcoholic Extract ◽  
Protective Effects ◽  
Myrtus Communis ◽  
Leaf Extracts

Myrtus communis Linn. (MC) is a cardiotonic plant in traditional Persian medicine. This study was conducted to evaluate the protective effect of MC on isoproterenol-induced heart failure (HF) in rats. Isoproterenol was injected subcutaneously in all groups except the control group for 4 consecutive days to induce myocardial injury in male Wistar rats. In the case of treatment groups, the animals were treated with different doses of the hydro-alcoholic extract of MC fruit or leaves (150, 300, and 700 mg/kg), and were compared with healthy and HF rats. In order to evaluate cardiac function, echocardiography was performed on day 28 after treatment. MC fruit and leaf extracts were administered to all groups except the healthy control group for 28 days by gavage. At the end of the experimental period, the animals were sacrificed and the left ventricle regions of tissue hearts were collected to measure the levels of oxidative stress factors (MDA, SOD, GSH) using ELISA methods. Cardiac fibrosis was evaluated by Mason’s trichrome staining. Hematoxylin-eosin staining was used to assess histopathological changes in cardiac structure.  Our results showed that administration of MC fruit and leaf extracts significantly reduced the MDA level and increased SOD and GSH levels in treated HF rats compared to the HF group (P<0.05). In addition, MC mitigated fibrosis and improved cardiac histological changes compared to the HF group. Collectively, our findings show that MC can be considered as a good candidate to provide cardioprotective effects in HF rats through reduction of oxidative stress and myocardial fibrosis.

scholarly journals Melatonin to Rescue the Aged Heart: Antiarrhythmic and Antioxidant Benefits

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Margarita Segovia-Roldan ◽  
Emiliano Raúl Diez ◽  
Esther Pueyo
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular System ◽  
Cardiac Arrhythmias ◽  
Protective Effects ◽  
Epigenetic Alterations ◽  
Structural Alterations ◽  
Telomere Attrition ◽  
Gradual Loss ◽  
Fountain Of Youth ◽  
Pleiotropic Actions

Aging comes with gradual loss of functions that increase the vulnerability to disease, senescence, and death. The mechanisms underlying these processes are linked to a prolonged imbalance between damage and repair. Damaging mechanisms include oxidative stress, mitochondrial dysfunction, chronodisruption, inflammation, and telomere attrition, as well as genetic and epigenetic alterations. Several endogenous tissue repairing mechanisms also decrease. These alterations associated with aging affect the entire organism. The most devastating manifestations involve the cardiovascular system and may lead to lethal cardiac arrhythmias. Together with structural remodeling, electrophysiological and intercellular communication alterations during aging predispose to arrhythmic events. Despite the knowledge on repairing mechanisms in the cardiovascular system, effective antiaging strategies able to reduce the risk of arrhythmias are still missing. Melatonin is a promising therapeutic candidate due to its pleiotropic actions. This indoleamine regulates chronobiology and endocrine physiology. Of relevance, melatonin is an antiaging, antioxidant, antiapoptotic, antiarrhythmic, immunomodulatory, and antiproliferative molecule. This review focuses on the protective effects of melatonin on age-induced cardiac functional and structural alterations, potentially becoming a new fountain of youth for the heart.

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