scholarly journals Physical Exercise: A Novel Tool to Protect Mitochondrial Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Daniela Sorriento ◽  
Eugenio Di Vaia ◽  
Guido Iaccarino
Keyword(s):  
Physical Exercise ◽  
Heart Diseases ◽  
Oxygen Species ◽  
Metabolic Abnormalities ◽  
Energetic Metabolism ◽  
Potential Therapeutic Target ◽  
Mitochondrial Quality Control ◽  
Factors Associated ◽  
And Function ◽  
Critical Process

Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect crucial homeostatic processes, such asATP production, the generation of reactive oxygen species, and the release of pro-apoptotic factors, associated with metabolic abnormalities. In response to energetic deficiency, the cardiomyocytes activate the Mitochondrial Quality Control (MQC), a critical process in maintaining mitochondrial health. This process is compromised in cardiovascular diseases depending on the pathology’s severity and represents, therefore, a potential therapeutic target. Several potential targeting molecules within this process have been identified in the last years, and therapeutic strategies have been proposed to ameliorate mitochondria monitoring and function. In this context, physical exercise is considered a non-pharmacological strategy to protect mitochondrial health. Physical exercise regulates MQC allowing the repair/elimination of damaged mitochondria and synthesizing new ones, thus recovering the metabolic state. In this review, we will deal with the effect of physical exercise on cardiac mitochondrial function tracing its ability to modulate specific steps in MQC both in physiologic and pathologic conditions.

scholarly journals The Combination of Physical Exercise with Muscle-Directed Antioxidants to Counteract Sarcopenia: A Biomedical Rationale for Pleiotropic Treatment with Creatine and Coenzyme Q10

2017 ◽  
Vol 2017 ◽  
pp. 1-19 ◽  
Author(s):  
Michele Guescini ◽  
Luca Tiano ◽  
Maria Luisa Genova ◽  
Emanuela Polidori ◽  
Sonia Silvestri ◽  
...  
Keyword(s):  
Public Health ◽  
Physical Exercise ◽  
Coenzyme Q10 ◽  
Ros Production ◽  
Oxygen Species ◽  
Risk Of Death ◽  
Increased Risk ◽  
Risk Of Falls ◽  
Muscle Impairment ◽  
And Function

Sarcopenia represents an increasing public health risk due to the rapid aging of the world’s population. It is characterized by both low muscle mass and function and is associated with mobility disorders, increased risk of falls and fractures, loss of independence, disabilities, and increased risk of death. Despite the urgency of the problem, the development of treatments for sarcopenia has lagged. Increased reactive oxygen species (ROS) production and decreased antioxidant (AO) defences seem to be important factors contributing to muscle impairment. Studies have been conducted to verify whether physical exercise and/or AOs could prevent and/or delay sarcopenia through a normalization of the etiologically relevant ROS imbalance. Despite the strong rationale, the results obtained were contradictory, particularly with regard to the effects of the tested AOs. A possible explanation might be that not all the agents included in the general heading of “AOs” could fulfill the requisites to counteract the complex series of events causing/accelerating sarcopenia: the combination of the muscle-directed antioxidants creatine and coenzyme Q10 with physical exercise as a biomedical rationale for pleiotropic prevention and/or treatment of sarcopenia is discussed.

scholarly journals Mitochondrial Bioenergetics and Turnover during Chronic Muscle Disuse

2021 ◽  
Vol 22 (10) ◽  
pp. 5179
Author(s):  
Jonathan M. Memme ◽  
Mikhaela Slavin ◽  
Neushaw Moradi ◽  
David A. Hood
Keyword(s):  
Bed Rest ◽  
Metabolic Health ◽  
Muscle Quality ◽  
Whole Body ◽  
Oxygen Species ◽  
Mitochondrial Quality Control ◽  
Muscle Disuse ◽  
Mitochondrial Alterations ◽  
And Function ◽  
Limb Immobilization

Periods of muscle disuse promote marked mitochondrial alterations that contribute to the impaired metabolic health and degree of atrophy in the muscle. Thus, understanding the molecular underpinnings of muscle mitochondrial decline with prolonged inactivity is of considerable interest. There are translational applications to patients subjected to limb immobilization following injury, illness-induced bed rest, neuropathies, and even microgravity. Studies in these patients, as well as on various pre-clinical rodent models have elucidated the pathways involved in mitochondrial quality control, such as mitochondrial biogenesis, mitophagy, fission and fusion, and the corresponding mitochondrial derangements that underlie the muscle atrophy that ensues from inactivity. Defective organelles display altered respiratory function concurrent with increased accumulation of reactive oxygen species, which exacerbate myofiber atrophy via degradative pathways. The preservation of muscle quality and function is critical for maintaining mobility throughout the lifespan, and for the prevention of inactivity-related diseases. Exercise training is effective in preserving muscle mass by promoting favourable mitochondrial adaptations that offset the mitochondrial dysfunction, which contributes to the declines in muscle and whole-body metabolic health. This highlights the need for further investigation of the mechanisms in which mitochondria contribute to disuse-induced atrophy, as well as the specific molecular targets that can be exploited therapeutically.

Focal Adhesion Kinase in Ovarian Cancer: A Potential Therapeutic Target for Platinum and Taxane-Resistant Tumors

2019 ◽  
Vol 19 (3) ◽  
pp. 179-188 ◽  
Author(s):  
Arkene Levy ◽  
Khalid Alhazzani ◽  
Priya Dondapati ◽  
Ali Alaseem ◽  
Khadijah Cheema ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Tumor Stage ◽  
Current Status ◽  
Potential Therapeutic Target ◽  
Resistant Disease ◽  
Development Of Resistance ◽  
And Function ◽  
Mdr 1

Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase, which is an essential player in regulating cell migration, invasion, adhesion, proliferation, and survival. Its overexpression and activation have been identified in sixty-eight percent of epithelial ovarian cancer patients and this is significantly associated with higher tumor stage, metastasis, and shorter overall survival of these patients. Most recently, a new role has emerged for FAK in promoting resistance to taxane and platinum-based therapy in ovarian and other cancers. The development of resistance is a complex network of molecular processes that make the identification of a targetable biomarker in platinum and taxane-resistant ovarian cancer a major challenge. FAK overexpression upregulates ALDH and XIAP activity in platinum-resistant and increases CD44, YB1, and MDR-1 activity in taxaneresistant tumors. FAK is therefore now emerging as a prognostically significant candidate in this regard, with mounting evidence from recent successes in preclinical and clinical trials using small molecule FAK inhibitors. This review will summarize the significance and function of FAK in ovarian cancer, and its emerging role in chemotherapeutic resistance. We will discuss the current status of FAK inhibitors in ovarian cancers, their therapeutic competencies and limitations, and further propose that the combination of FAK inhibitors with platinum and taxane-based therapies could be an efficacious approach in chemotherapeutic resistant disease.

Identification of transcription factors associated with castration-resistance: Is the serum responsive factor a potential therapeutic target?

The Prostate ◽  
2013 ◽  
Vol 73 (7) ◽  
pp. 743-753 ◽  
Author(s):  
Maria Prencipe ◽  
Stephen F. Madden ◽  
Amanda O'Neill ◽  
Gillian O'Hurley ◽  
Aedin Culhane ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Therapeutic Target ◽  
Castration Resistance ◽  
Potential Therapeutic Target ◽  
Factors Associated

scholarly journals Molecular Characterization of Reactive Oxygen Species in Myocardial Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Tingyang Zhou ◽  
Chia-Chen Chuang ◽  
Li Zuo
Keyword(s):  
Reactive Oxygen Species ◽  
Myocardial Ischemia ◽  
Energy Demand ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
High Energy ◽  
Protective Mechanism ◽  
Oxygen Species ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia-reperfusion (I/R) injury is experienced by individuals suffering from cardiovascular diseases such as coronary heart diseases and subsequently undergoing reperfusion treatments in order to manage the conditions. The occlusion of blood flow to the tissue, termed ischemia, can be especially detrimental to the heart due to its high energy demand. Several cellular alterations have been observed upon the onset of ischemia. The danger created by cardiac ischemia is somewhat paradoxical in that a return of blood to the tissue can result in further damage. Reactive oxygen species (ROS) have been studied intensively to reveal their role in myocardial I/R injury. Under normal conditions, ROS function as a mediator in many cell signaling pathways. However, stressful environments significantly induce the generation of ROS which causes the level to exceed body’s antioxidant defense system. Such altered redox homeostasis is implicated in myocardial I/R injury. Despite the detrimental effects from ROS, low levels of ROS have been shown to exert a protective effect in the ischemic preconditioning. In this review, we will summarize the detrimental role of ROS in myocardial I/R injury, the protective mechanism induced by ROS, and potential treatments for ROS-related myocardial injury.

scholarly journals Glutathione Participation in the Prevention of Cardiovascular Diseases

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1220
Author(s):  
Deyamira Matuz-Mares ◽  
Héctor Riveros-Rosas ◽  
María Magdalena Vilchis-Landeros ◽  
Héctor Vázquez-Meza
Keyword(s):  
Cardiovascular Diseases ◽  
Superoxide Anion ◽  
Reactive Nitrogen Species ◽  
Hypochlorous Acid ◽  
Reduced Glutathione ◽  
Heart Diseases ◽  
Reactive Species ◽  
Oxygen Species ◽  
Cardiovascular Pathologies

Cardiovascular diseases (CVD) (such as occlusion of the coronary arteries, hypertensive heart diseases and strokes) are diseases that generate thousands of patients with a high mortality rate worldwide. Many of these cardiovascular pathologies, during their development, generate a state of oxidative stress that leads to a deterioration in the patient’s conditions associated with the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Within these reactive species we find superoxide anion (O2•–), hydroxyl radical (•OH), nitric oxide (NO•), as well as other species of non-free radicals such as hydrogen peroxide (H2O2), hypochlorous acid (HClO) and peroxynitrite (ONOO–). A molecule that actively participates in counteracting the oxidizing effect of reactive species is reduced glutathione (GSH), a tripeptide that is present in all tissues and that its synthesis and/or regeneration is very important to be able to respond to the increase in oxidizing agents. In this review, we will address the role of glutathione, its synthesis in both the heart and the liver, and its importance in preventing or reducing deleterious ROS effects in cardiovascular diseases.

Abstract 207: Unc-51-like Kinase 1 (ULK1) Plays A Crucial Role In Mitophagy In Cardiomyocytes

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Toshiro Saito ◽  
Junichi Sadoshima
Keyword(s):  
Glucose Deprivation ◽  
High Ratio ◽  
Control Mechanisms ◽  
Oxygen Species ◽  
Predominant Role ◽  
Mitochondrial Quality Control ◽  
Over Expression ◽  
Pathological Conditions

The mitochondrion is an essential organelle that supplies ATP in cardiomyocytes (CMs). However, damaged mitochondria are harmful via the production of reactive oxygen species and induction of apoptosis in pathological conditions. Therefore, quality of mitochondria should be controlled tightly through various mitochondrial quality control mechanisms. Mitochondrial autophagy (mitophagy) is considered an integral part of this mechanism, and recent investigations uncovered the role of PINK1 and Parkin in mitophagy. However, these observations were made under artificial conditions, such as over-expression of Parkin or treatment with CCCP, and thus the precise mechanism has not been fully elucidated in more pathophysiologically relevant conditions. Recent evidence suggests that mitophagy can take place independently of ATG7, a molecule essential for the conventional form of autophagy, and that this form of autophagy is ULK1-dependent. We investigated the role of ULK1 and ATG7 in mediating mitophagy using mitochondria-targeted Keima (Mito-Keima) in cultured rat neonatal CMs. Keima has a bimodal excitation spectrum peaking at 440 and 560 nm, corresponding to the neutral and acidic pH, respectively. In CMs transfected with Mito-Keima, the fluorescent dots with a high 560nm/440nm ratio represent the mitochondria incorporated into autolysosomes which indicate mitophagy. Here we report that ULK1 plays a more predominant role in glucose deprivation (GD) -induced mitophagy than ATG7. Control CMs exhibited 8.7±1.0 % of the area of high-ratio dots per cells after GD. Knockdown of ULK1 significantly reduced the area to 2.3±0.9 % in CMs after GD (p<0.01, vs sh-Control). The reduction was significantly greater in CMs with knockdown of ULK1 than that of ATG7 (7.0±1.6 %, p<0.05, sh-ULK1 vs sh-ATG7). In addition, knockdown of Beclin1 and Drp1 also significantly decreased the area of high-ratio dots (about 1.0 % and 0.5 %, respectively). Overexpression of ULK1 was sufficient to induce mitophagy without starvation, whereas that of ATG7 was not. These results suggest that ULK1, Beclin1 and Drp1 play an essential role in mediating GD-induced mitophagy in CMs.

The impact of physical exercise on the occurence of arrhythmias in athletes – recommendations

2018 ◽  
Vol 1 (46) ◽  
pp. 11-15
Author(s):  
Jakub Szwed ◽  
Michał Kowara ◽  
Marcin Grabowski
Keyword(s):  
Physical Exercise ◽  
Heart Diseases ◽  
Sudden Cardiac Arrest ◽  
Endurance Sports ◽  
Endurance Sport ◽  
Sport Training ◽  
Negative Results ◽  
Structural Heart Diseases ◽  
Long Time ◽  
The Impact

The aim of this article is to demonstrate the impact of physical exercise on the development of arrhytmias in athletes. The studies show that this relation exist and concerns endurance sports practiced for a long time. In addition, this article contains review of the most common arrhythmias in athletes and appropriate recommendations. The time of arrhythmias onset depends on the presence of structural heart diseases. If the cardiac disorder is absent the arrhythmias appear at the age 40-50. If the structural heart diseases exist, the arrhythmias occur in young athletes and are more dangerous (can lead to sudden cardiac arrest). The most common arrhythmia in endurance athletes is atrial fibrillation. In order to avoid negative results of endurance sports, such as cardiac arrhythmias, the reliable examinations are necessary, especially to exclude structural cardiac diseases. These examinations should be undertaken before initiation of endurance sport training and routinely later, in course of follow-up.

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