Mitochondrial biogenesis in hereditary optic neuropathies

Шеремет, Н Л; Andreeva, N.A.; Shmelkova, M.S.; Tsigankova, P. G.

doi:10.17116/oftalma201913505185

Cited by 4 publications

(1 citation statement)

References 44 publications

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“…Some scholars evaluate the biogenesis of mitochondria by measuring the rate of mitochondrial protein synthesis. Mitochondrial biogenesis and mitophagy coordinately regulate the molecular mechanism of mitochondrial homeostasis (101)(102)(103)(104). On the one hand, the process of mitochondrial biogenesis is accompanied by mitophagy, on the other hand, abnormal mitophagy can feedback and inhibit mitochondrial biogenesis, and the PGC-1α-NRF1-FUNDC1 pathway plays a key role in it, cooperating to maintain the quality and quantity of mitochondria (96,97,105,106).…”

Section: Biogenesismentioning

confidence: 99%

Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

Yin

Shen

2021

Front. Cardiovasc. Med.

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Mitochondria are the most abundant organelles in cardiac cells, and are essential to maintain the normal cardiac function, which requires mitochondrial dynamics and mitophagy to ensure the stability of mitochondrial quantity and quality. When mitochondria are affected by continuous injury factors, the balance between mitochondrial dynamics and mitophagy is broken. Aging and damaged mitochondria cannot be completely removed in cardiac cells, resulting in energy supply disorder and accumulation of toxic substances in cardiac cells, resulting in cardiac damage and cardiotoxicity. This paper summarizes the specific underlying mechanisms by which various adverse factors interfere with mitochondrial dynamics and mitophagy to produce cardiotoxicity and emphasizes the crucial role of oxidative stress in mitophagy. This review aims to provide fresh ideas for the prevention and treatment of cardiotoxicity induced by altered mitochondrial dynamics and mitophagy.

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Section: Biogenesismentioning

confidence: 99%

Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

Yin

Shen

2021

Front. Cardiovasc. Med.

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Characteristics of changes in retinal and optic nerve microvascularisature in Leber hereditary optic neuropathy patients seen with optical coherence tomography angiography

Шеремет¹,

Shmelkova²,

Andreeva³

et al. 2020

Vestn. oftal'mol.

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The Role of Mitophagy in Hereditary Optic Neuropathies. Literature Review

Andreeva¹,

Sheremet²,

Мураховская³

et al. 2021

Oftalʹmologiâ

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The role of mitophagy in hereditary optic neuropathies is considering in this review. Mitochondria are intracellular double membrane organelles. They are one of the main components of all eukaryotic cells, they perform many different functions in the cell. However, the main function of mitochondria is to supply cells with energy in the form of ATP. The ATP synthesis is carried out due to the respiratory chain five protein complexes work, the main components of the chain are located in the inner mitochondrial membrane. It is known that proteins that form all respiratory chain complexes (except II) are encoded by both nuclear and mitochondrial genes. The mitochondrial electron transport chain dysfunction leads to the mitochondrial diseases development, which can be a result of mutations both in mtDNA and in nDNA. The most common eye mitochondrial diseases are hereditary optic neuropathies (HON), such as Leber Hereditary Optic Neuropathy (LHON). The main cause leading to the disease are mtDNA mutations. These mutations lead to the respiratory chain complexes dysfunction (mainly I), which results in mitochondrial damage. To remove damaged mitochondria in time, cells have special regulatory systems. These systems are responsible for the damaged mitochondria detection, isolation and degradation through a specific form of autophagy, mitophagy. For normal functioning, cells need to maintain a constant balance between mitochondrial biogenesis and mitophagy. A violation of this balance leads to the disease. It was revealed that mitophagy, an important retinal ganglion cells protection mechanism, is impaired in patients with LHON. The mitophagy activation may have the therapeutic potential. Some pharmacological agents activate mitophagy and thereby slow down the disease development in patients with hereditary optic neuropathies, such as LHON. Some of them, such as rapamycin, trehalose, metformin, spermidine, NAD+ , are described in the review.

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Mitochondrial biogenesis in hereditary optic neuropathies

Cited by 4 publications

References 44 publications

Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

Characteristics of changes in retinal and optic nerve microvascularisature in Leber hereditary optic neuropathy patients seen with optical coherence tomography angiography

The Role of Mitophagy in Hereditary Optic Neuropathies. Literature Review

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