The Mitochondrion as a Key Regulator of Ischaemic Tolerance and Injury

Silachev, D. N.; Plotnikov, Egor Y.; Pevzner, Irina B.; Zorova, Ljubava D.; Babenko, Valentina A.; Zorov, Savva D.; Popkov, Vasily A.; Jankauskas, Stanislovas S.; Зинченко, В. П.; Сухих, Г. Т.; Zorov, Dmitry B.

doi:10.1016/j.hlc.2014.05.022

Cited by 43 publications

(30 citation statements)

References 66 publications

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“…The researchers observed abnormal patterns of mitochondrial respiration, decreased mitochondrial respiratory complex activity (complex II), decreased mitochondrial membrane potential, insufficient adenosine triphosphate production, and subsequent bioenergetic dysfunction using heart tissue cubes from mice after acute particulate matter exposure. Mitochondria also play an important role in ischemic preconditioning by repeatedly releasing small doses of ROS so that specific organs, including the myocardium, can acquire greater tolerance to larger and persistent ischemic injury [84]. Damage to the pre-protective mechanism of myocardium during ischemic injury may potentially exacerbate myocardial damage in ACS.…”

Section: Potential Cellular and Molecular Biology Mechanismsmentioning

confidence: 99%

“…An inadequate energy supply to heart tissue after exposure to PM 2.5 may be through several feasible mechanisms: (1) an increased demand for energy could be induced by an increased heart rate and arrhythmia triggered by PM 2.5 exposure [97]; (2) insufficient blood perfusion to the heart may result from defective vasomotor regulation [98,99] resulting in ineffective diastole from secondary tachyarrhythmia; and (3) acute damage to the mitochondrial respiratory chain will result in reduced production of adenosine triphosphate [83], which serves as a direct source of energy for heart tissue, resulting in an insufficient energy supply to the heart and a diminished threshold for myocardial ischemia [84,100]. The combined effect of increased consumption and an inadequate supply of energy will promote the onset and development of ACS.…”

Section: Potential Physiopathologic Mechanisms Mediating Pm25-indmentioning

confidence: 99%

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Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Meng

Zhang

Yang

et al. 2016

IJERPH

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The harmful effects of particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) and its association with acute coronary syndrome (ACS) has gained increased attention in recent years. Significant associations between PM2.5 and ACS have been found in most studies, although sometimes only observed in specific subgroups. PM2.5-induced detrimental effects and ACS arise through multiple mechanisms, including endothelial injury, an enhanced inflammatory response, oxidative stress, autonomic dysfunction, and mitochondria damage as well as genotoxic effects. These effects can lead to a series of physiopathological changes including coronary artery atherosclerosis, hypertension, an imbalance between energy supply and demand to heart tissue, and a systemic hypercoagulable state. Effective strategies to prevent the harmful effects of PM2.5 include reducing pollution sources of PM2.5 and population exposure to PM2.5, and governments and organizations publicizing the harmful effects of PM2.5 and establishing air quality standards for PM2.5. PM2.5 exposure is a significant risk factor for ACS, and effective strategies with which to prevent both susceptible and healthy populations from an increased risk for ACS have important clinical significance in the prevention and treatment of ACS.

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Section: Potential Cellular and Molecular Biology Mechanismsmentioning

confidence: 99%

Section: Potential Physiopathologic Mechanisms Mediating Pm25-indmentioning

confidence: 99%

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Meng

Zhang

Yang

et al. 2016

IJERPH

View full text Add to dashboard Cite

show abstract

“…One possible mechanism of the neuroprotective action of antioxidant derivatives of plastoquinone is the prevention of OS due to soft separation and prevention of mitochondrial hyperpolarization. [72][73][74] Except for ischemia, the inhibitory effect of preparations of the SkQ family on damage in the nervous tissue has been demonstrated in different models of Alzheimer's disease (including ex vivo), [60,[75][76][77][78] as well as in the model of agerelated retinopathy. [51] In the work, [79] an oral supplementation of SkQ1 with food for 2-3 weeks on the magnitude of ischemic and reperfusion injury of the heart was studied under male rats.…”

Section: Mitochondria-targeted Antioxidants: Development and Effectivmentioning

confidence: 99%

Untitled

Tkachova¹

2018

AJP

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There is presented the outcome analysis of numerous studies on the mechanisms of oxidative stress (OS) associated with increasing of the generation of reactive oxygen intermediate (ROI) in the electronic transport circuit of mitochondria, as well as the effect of ROI on the level of mutations in mitochondrial DNA (mtDNA). It is shown a fine sensibility of mtDNA to oxidative affections and mutations. The relation of age accumulation of mtDNA mutations with aging and life expectancy has been noted. It is also shown the relationship of OS with mtDNA mutations, apoptosis, diseases, and aging. It is considered a pharmacological way for the protection of ROI, aging, diseases, and prolonging life with the help of the antioxidant SkQ1, addressed directly to the mitochondria.

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“…These ROS are thought to "…activate local pools of redox-sensitive enzymes," in order to "… limit ischemic damage to cells in that area." [57] The role of mitochondrial ROS is emphasized by Silachev et al [58]:…”

Section: Adaptive Stress Response Cross-resistance and Preconditioningmentioning

confidence: 99%

Oxy-nitroso shielding burst model of cold atmospheric plasma therapeutics

Graves

2014

Clinical Plasma Medicine

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Cite this article as: David B Graves, Oxy-nitroso shielding burst model of cold atmospheric plasma therapeutics, Clinical Plasma Medicine, http://dx. AbstractIt is postulated that cold atmospheric plasma (CAP) can trigger a therapeutic shielding response in tissue by creating a time-and space-localized, burst-like form of oxy-nitrosative stress on near-surface exposed cells through the flux of plasma-generated reactive oxygen and nitrogen species (RONS). RONS-exposed surface layers of cells communicate to the deeper levels of tissue via a form of the 'bystander effect,' similar to responses to other forms of cell stress. In this proposed model of CAP therapeutics, the plasma stimulates a cellular survival mechanism through which aerobic organisms shield themselves from infection and other challenges.

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The Mitochondrion as a Key Regulator of Ischaemic Tolerance and Injury

Cited by 43 publications

References 66 publications

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Potential Harmful Effects of PM2.5 on Occurrence and Progression of Acute Coronary Syndrome: Epidemiology, Mechanisms, and Prevention Measures

Untitled

Oxy-nitroso shielding burst model of cold atmospheric plasma therapeutics

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