scholarly journals The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes

2021 ◽  
Vol 8 ◽  
Author(s):  
Olga A. Zhunina ◽  
Nikita G. Yabbarov ◽  
Andrey V. Grechko ◽  
Antonina V. Starodubova ◽  
Ekaterina Ivanova ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Protein ◽  
Cellular Damage ◽  
Future Perspective ◽  
Antioxidant Systems ◽  
Mtdna Damage ◽  
Mtdna Mutations ◽  
Wide Range

Mitochondrial dysfunction is known to be associated with a wide range of human pathologies, such as cancer, metabolic, and cardiovascular diseases. One of the possible ways of mitochondrial involvement in the cellular damage is excessive production of reactive oxygen and nitrogen species (ROS and RNS) that cannot be effectively neutralized by existing antioxidant systems. In mitochondria, ROS and RNS can contribute to protein and mitochondrial DNA (mtDNA) damage causing failure of enzymatic chains and mutations that can impair mitochondrial function. These processes further lead to abnormal cell signaling, premature cell senescence, initiation of inflammation, and apoptosis. Recent studies have identified numerous mtDNA mutations associated with different human pathologies. Some of them result in imbalanced oxidative phosphorylation, while others affect mitochondrial protein synthesis. In this review, we discuss the role of mtDNA mutations in cancer, diabetes, cardiovascular diseases, and atherosclerosis. We provide a list of currently described mtDNA mutations associated with each pathology and discuss the possible future perspective of the research.

scholarly journals The Role of Mitochondria in Cardiovascular Diseases

Biology ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 137 ◽  
Author(s):  
Anastasia V. Poznyak ◽  
Ekaterina A. Ivanova ◽  
Igor A. Sobenin ◽  
Shaw-Fang Yet ◽  
Alexander N. Orekhov
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Mitochondrial Dysfunction ◽  
Energy Production ◽  
Cardiovascular Disorders ◽  
Intensive Study ◽  
Potential Therapeutic Target ◽  
Cell Dysfunction ◽  
Mtdna Mutations

The role of mitochondria in cardiovascular diseases is receiving ever growing attention. As a central player in the regulation of cellular metabolism and a powerful controller of cellular fate, mitochondria appear to comprise an interesting potential therapeutic target. With the development of DNA sequencing methods, mutations in mitochondrial DNA (mtDNA) became a subject of intensive study, since many directly lead to mitochondrial dysfunction, oxidative stress, deficient energy production and, as a result, cell dysfunction and death. Many mtDNA mutations were found to be associated with chronic human diseases, including cardiovascular disorders. In particular, 17 mtDNA mutations were reported to be associated with ischemic heart disease in humans. In this review, we discuss the involvement of mitochondrial dysfunction in the pathogenesis of atherosclerosis and describe the mtDNA mutations identified so far that are associated with atherosclerosis and its risk factors.

Role of nitric oxide-induced mtDNA damage in mitochondrial dysfunction and apoptosis

2006 ◽  
Vol 40 (5) ◽  
pp. 754-762 ◽  
Author(s):  
Lyudmila I. Rachek ◽  
Valentina I. Grishko ◽  
Susan P. LeDoux ◽  
Glenn L. Wilson
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Dysfunction ◽  
Mtdna Damage

scholarly journals Evolving Role of Microparticles in the Pathophysiology of Endothelial Dysfunction

2013 ◽  
Vol 59 (8) ◽  
pp. 1166-1174 ◽  
Author(s):  
Fina Lovren ◽  
Subodh Verma
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Vascular Endothelial Cells ◽  
Current Knowledge ◽  
Early Event ◽  
Prognostic Information ◽  
Vascular Events ◽  
Wide Range

BACKGROUND Endothelial dysfunction is an early event in the development and progression of a wide range of cardiovascular diseases. Various human studies have identified that measures of endothelial dysfunction may offer prognostic information with respect to vascular events. Microparticles (MPs) are a heterogeneous population of small membrane fragments shed from various cell types. The endothelium is one of the primary targets of circulating MPs, and MPs isolated from blood have been considered biomarkers of vascular injury and inflammation. CONTENT This review summarizes current knowledge of the potential functional role of circulating MPs in promoting endothelial dysfunction. Cells exposed to different stimuli such as shear stress, physiological agonists, proapoptotic stimulation, or damage release MPs, which contribute to endothelial dysfunction and the development of cardiovascular diseases. Numerous studies indicate that MPs may trigger endothelial dysfunction by disrupting production of nitric oxide release from vascular endothelial cells and subsequently modifying vascular tone. Circulating MPs affect both proinflammatory and proatherosclerotic processes in endothelial cells. In addition, MPs can promote coagulation and inflammation or alter angiogenesis and apoptosis in endothelial cells. SUMMARY MPs play an important role in promoting endothelial dysfunction and may prove to be true biomarkers of disease state and progression.

scholarly journals Impairment between Oxidant and Antioxidant Systems: Short- and Long-term Implications for Athletes’ Health

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1353 ◽  
Author(s):  
Cristina Nocella ◽  
Vittoria Cammisotto ◽  
Fabio Pigozzi ◽  
Paolo Borrione ◽  
Chiara Fossati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Exercise Training ◽  
Muscle Damage ◽  
Neurological Diseases ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Oxidative Balance

The role of oxidative stress, an imbalance between reactive oxygen species production (ROS) and antioxidants, has been described in several patho-physiological conditions, including cardiovascular, neurological diseases and cancer, thus impacting on individuals’ lifelong health. Diet, environmental pollution, and physical activity can play a significant role in the oxidative balance of an organism. Even if physical training has proved to be able to counteract the negative effects caused by free radicals and to provide many health benefits, it is also known that intensive physical activity induces oxidative stress, inflammation, and free radical-mediated muscle damage. Indeed, variations in type, intensity, and duration of exercise training can activate different patterns of oxidant–antioxidant balance leading to different responses in terms of molecular and cellular damage. The aim of the present review is to discuss (1) the role of oxidative status in athletes in relation to exercise training practice, (2) the implications for muscle damage, (3) the long-term effect for neurodegenerative disease manifestations, (4) the role of antioxidant supplementations in preventing oxidative damages.

Iron Oxide Nanoparticles as Imaging and Therapeutic Agents for Atherosclerosis

2020 ◽  
Vol 46 (05) ◽  
pp. 553-562
Author(s):  
Joshua Talev ◽  
Jagat Rakesh Kanwar
Keyword(s):  
Iron Oxide ◽  
Cardiovascular Diseases ◽  
Iron Oxide Nanoparticles ◽  
Imaging Techniques ◽  
Therapeutic Agents ◽  
Oxide Nanoparticles ◽  
Future Prospects ◽  
Wide Range ◽  
Theranostic Applications

AbstractAtherosclerosis is the major cause of cardiovascular diseases and is the leading cause of mortality worldwide. Iron oxide nanoparticles have emerged as potential diagnostic and therapeutic agents for a wide range of conditions. To date, the theranostic applications of iron oxide nanoparticles have been studied mainly in cancer, but atherosclerosis has not received the same attention. Therefore, it appears appropriate to review the current and future applications of iron oxide nanoparticles for the diagnosis and therapy of atherosclerosis. This review will first discuss current imaging techniques for the diagnosis of atherosclerosis as well as their limitations. It will then discuss the role of nanotechnology for molecular imaging of atherosclerosis and the benefits of this approach as well as reviewing current developments in the field including single, bi-, and tri-modal imaging. Next, it will discuss the role of nanotechnology for therapies of atherosclerosis with a focus on nanotheranostics, concluding with a look at the challenges faced by nanoparticle-based imaging and therapy of atherosclerosis as well as a look at future prospects.

scholarly journals Chronically elevated glucose compromises myocardial mitochondrial DNA integrity by alteration of mitochondrial topoisomerase function

2011 ◽  
Vol 300 (2) ◽  
pp. C338-C348 ◽  
Author(s):  
S. Medikayala ◽  
B. Piteo ◽  
X. Zhao ◽  
J. G. Edwards
Keyword(s):  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Dna Cleavage ◽  
Experimental Period ◽  
Well Being ◽  
Dna Integrity ◽  
Mtdna Damage ◽  
Mtdna Mutations ◽  
Underlying Basis ◽  
Elevated Glucose

Mitochondrial dysfunction has a significant role in the development and complications of diabetic cardiomyopathy. Mitochondrial dysfunction and mitochondrial DNA (mtDNA) mutations are also associated with different types of cancer and neurodegenerative diseases. The goal of this study was to determine if chronically elevated glucose increase in mtDNA damage contributed to mitochondrial dysfunction and identify the underlying basis for mtDNA damage. H9c2 myotubes (a cardiac-derived cell line) were studied in the presence of 5.5, 16.5, or 33.0 mM glucose for up to 13 days. Tests of mitochondria function (Complex I and IV activity and ATP generation) were all significantly depressed by elevated media glucose. Intramitochondrial superoxide and intracellular superoxide levels were transiently increased during the experimental period. AnnexinV binding (a marker of apoptosis) was significantly increased after 7 and 13 days of high glucose. Thirteen days of elevated glucose significantly increased mtDNA damage globally and across the region encoding for the three subunits of cytochrome oxidase. Using mitochondria isolated from cells chronically exposed to elevated glucose, we observed significant increases in topoisomerase-linked DNA cleavage. Mitochondria-dependent DNA cleavage was significantly exacerbated by H2O2 and that immunoprecipitation of mitochondrial extracts with a mtTOP1 antibody significantly decreased DNA cleavage, indicating that at least part of this activity could be attributed to mtTOP1. We conclude that even mild increases in glucose presentation compromised mitochondrial function as a result of a decline in mtDNA integrity. Separate from a direct impact of oxidative stress on mtDNA, ROS-induced alteration of mitochondrial topoisomerase activity exacerbated and propagated increases in mtDNA damage. These findings are significant in that the activation/inhibition state of the mitochondrial topoisomerases will have important consequences for mitochondrial DNA integrity and the well being of the myocardium.

Emerging role of SIRT3 in mitochondrial dysfunction and cardiovascular diseases

2018 ◽  
Vol 53 (2) ◽  
pp. 139-149 ◽  
Author(s):  
Jie Wu ◽  
Zhenhua Zeng ◽  
Weijin Zhang ◽  
Zhiya Deng ◽  
Yahui Wan ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Mitochondrial Dysfunction

scholarly journals Oxidative Stress and Epilepsy: Literature Review

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Carlos Clayton Torres Aguiar ◽  
Anália Barbosa Almeida ◽  
Paulo Victor Pontes Araújo ◽  
Rita Neuma Dantas Cavalcante de Abreu ◽  
Edna Maria Camelo Chaves ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Mitochondrial Dysfunction ◽  
Experimental Studies ◽  
Cellular Damage ◽  
Brain Disorder ◽  
Chronic Oxidative Stress ◽  
Seizure Models ◽  
And Oxidative Stress

Backgrounds. The production of free radicals has a role in the regulation of biological function, cellular damage, and the pathogenesis of central nervous system conditions. Epilepsy is a highly prevalent serious brain disorder, and oxidative stress is regarded as a possible mechanism involved in epileptogenesis. Experimental studies suggest that oxidative stress is a contributing factor to the onset and evolution of epilepsy.Objective. A review was conducted to investigate the link between oxidative stress and seizures, and oxidative stress and age as risk factors for epilepsy. The role of oxidative stress in seizure induction and propagation is also discussed.Results/Conclusions. Oxidative stress and mitochondrial dysfunction are involved in neuronal death and seizures. There is evidence that suggests that antioxidant therapy may reduce lesions induced by oxidative free radicals in some animal seizure models. Studies have demonstrated that mitochondrial dysfunction is associated with chronic oxidative stress and may have an essential role in the epileptogenesis process; however, few studies have shown an established link between oxidative stress, seizures, and age.

scholarly journals Nutraceuticals against Oxidative Stress in Autoimmune Disorders

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 261
Author(s):  
Carmen Mannucci ◽  
Marco Casciaro ◽  
Emanuela Elisa Sorbara ◽  
Fabrizio Calapai ◽  
Eleonora Di Salvo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fruits And Vegetables ◽  
Autoimmune Disorders ◽  
Chronic Illnesses ◽  
Antioxidant Systems ◽  
Oxidative Stress Biomarkers ◽  
Positive Effects ◽  
Dietary Antioxidant ◽  
Wide Range

Antioxidant mechanisms are constituted of enzymes, endogenous, and non-enzymatic, exogenous, which have the role of counterbalancing oxidative stress. Intake of these compounds occurs in the diet. Vegetables, plants, and fruits contain a wide range of alkaloids, polyphenols, and terpenoids which are called “phytochemicals”. Most of these substances are responsible for the positive properties of fruits and vegetables, which are an essential part of a healthy life with roles in ameliorating chronic illnesses and favoring longevity. Nutraceuticals are substances contained in a food or fragment of it influencing health with positive effects on health helping in precenting or treating disorders. We conducted a review illustrating the principal applications of nutraceuticals in autoimmune disorders. Literature reported several studies about exogenous dietary antioxidant supplementation in diverse autoimmune diseases such as rheumatoid arthritis, lupus, diabetes, and multiple sclerosis. In these pathologies, promising results were obtained in some cases. Positive outcomes were generally associated with a reduction of oxidative stress parameters and a boost to antioxidant systems, and sometimes with anti-inflammatory effects. The administration of exogenous substances through food derivates or dietary supplements following scientific standardization was demonstrated to be effective. Further bias-free and extended studies should be conducted that include ever-increasing oxidative stress biomarkers.

scholarly journals The role of perivascular adipose tissue in the development of cardiovascular diseases. The importance of diagnosis for assessing the risk stratification of cardiovascular diseases

2019 ◽  
Vol 91 (4) ◽  
pp. 130-135
Author(s):  
E G Uchasova ◽  
O V Gruzdeva ◽  
Yu A Dyleva ◽  
E V Belik
Keyword(s):  
Adipose Tissue ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
Physiological State ◽  
Biological Significance ◽  
Cellular Tissue ◽  
Perivascular Adipose Tissue ◽  
Fat Depots ◽  
Wide Range

Obesity is closely associated with metabolic and cardiovascular diseases, including dyslipidemia, coronary artery disease, hypertension, and heart failure. Adipose tissue (AT) is identified as a complex endocrine organ, with a wide range of regulatory functions at the cellular, tissue and systemic levels. Various terms, including paracardiac, epicardial and pericardial, are used to describe the fatty deposits surrounding the heart. Among all the fat depots, perivascular AT (PVAT) is of great biological significance for the cardiovascular system due to its anatomical proximity to the vessels. Recent studies have shown the presence of a complex, bidirectional paracrine and vasocardial signaling system between the vascular wall and PVAT. In the review, we will discuss the biological role of PVAT in both the physiological state and cardiovascular pathology, emphasizing its dual proatherogenic and antiatherogenic role. Let us consider PVAT as a target for various therapeutic agents in cardiovascular diseases. We will also analyze data on the role of non-invasive techniques as a diagnostic tool for assessing coronary artery inflammation.

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