The regulatory role of mitochondrial pora and the possibility of its pharmacological modulation

Pozhilova, Yelena Vasilyevna; Новиков, В. Е.; Левченкова, О. С.

doi:10.17816/rcf12313-19

Cited by 13 publications

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“…Cardiomyocyte apoptosis is mediated by the release of reactive oxygen species (ROS) and oxidative stress [2], mitochondrial and endothelial dysfunction. The calcium overload is also involved in the formation of the ROS pool [5] and in the blockade of the mitochondrial pore [10]. The mitochondrial pore is a channel that plays a significant role in the calcium metabolism between the mitochondria and the medium and can initiate the process of cellular degradation.…”

Section: I T E R a T U R E R E V I E Wmentioning

confidence: 99%

Anthracycline cardiomyopathy in anesthesiology

Lezhnev¹,

Paramonov²,

Solontsov³

et al. 2019

AREM

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Section: I T E R a T U R E R E V I E Wmentioning

confidence: 99%

Anthracycline cardiomyopathy in anesthesiology

Lezhnev¹,

Paramonov²,

Solontsov³

et al. 2019

AREM

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“…The knowledge about mitochondria is being constantly supplementated and expanded [30,42,49,51]. The diseases, based on hereditarily determined (primary) or acquired (secondary) mitochondrial dysfunction which was the disruption of energy production as ATP in the process of oxidative phosphorylation, have been detected [17,26,36,38].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunctions and antihypoxants

Новиков

Левченкова

Ivantsova

et al. 2020

Rev Clin Pharm Drug Ther

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Mitochondrial dysfunctions (an impaired energy metabolism in the mitochondria) are essential in a pathogenesis of many diseases. Aim. The analysis of various mitochondrial dysfunction (MD) type study, as well as evaluation of drugs with an antihypoxic effect in their treatment. Methods. Collection, systematization and analysis of experimental and clinical data of current scientific research about the problem. Results. The mitochondrial dysfunctions can be caused by genetic disorders of the mitochondrial or nuclear genome (the primary MD or the mitochondrial diseases), as well as structural, functional and biochemical defects of mitochondria caused by other diseases (the secondary MD). MD are characterized by impaired tissue respiration, ATP synthesis deficiency and decreased energy metabolism. The clinical implications of MD are polysystemic and polymorphic. One of the biochemical sign of MD is the lactic acidosis. There are certain difficulties with the early diagnosis of primary MD. It is suggested to use complete exome sequencing among patients with a clinical suspicion on mitochondrial disease. The energotropic pharmacotherapy including drugs with an antihypoxic effect is used for MD treatment. It is more rational to use the drug combination that influences different stages of energy production. The combinations of L-carnitine, coenzyme Q10, cytochrome C and succinate-containing drugs are frequently used for MD. However, the usage of energotropic and antihypoxic drugs is not able to cure the patients and stop the progression of all disease displays. Conclusion. MD are a multidisciplinary problem, therefore, doctors of any speciality must be competent in the MD diagnosis and treatment. The use of energotropic agents in the MD treatment requires further research. Numerous issues remain open (daily drug doses choice, treatment duration, rational combinations). The phenotype variability and the uniqueness of diagnosed cases, clinical and genetic differences between patient groups with mitochondrial diseases fail to create homogeneous samplings for therapy effectiveness and safety analysis. The literature data are the results of different degrees of reliability. The international efforts are needed to unify studies of related mitochondrial disorders, which, in combination with a constant improvement of MD pathogenesis knowledge will allow to develop more effective treatment regimens.

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2022

Mitochondria as a Key Intracellular Target of Thallium Toxicity

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The regulatory role of mitochondrial pora and the possibility of its pharmacological modulation

Cited by 13 publications

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Anthracycline cardiomyopathy in anesthesiology

Anthracycline cardiomyopathy in anesthesiology

Mitochondrial dysfunctions and antihypoxants

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