The Role of Mitochondrial miRNAs in the Development of Radon-Induced Lung Cancer

Kussainova, Assiya; Bulgakova, Olga; Aripova, Akmaral; Khalid, Zumama; Bersimbaev, R. I.; Izzotti, Alberto

doi:10.3390/biomedicines10020428

Cited by 11 publications

(7 citation statements)

References 162 publications

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“…Reports suggest that miR-1974, miR-1977, and miR-1978 may be transcribed directly from mtDNA (Bandiera et al, 2011;Barrey et al, 2011;Sripada et al, 2012;Kim et al, 2017). Supporting this notion, the sequences of certain pre-miRNAs and mature miRNAs-such as pre-miR-let7 and pre-miR-302a, which have been identified in human Frontiers in Physiology frontiersin.org muscle mitochondria-show alignment with the mitochondrial genome, hinting at the possibility of intramitochondrial mitomiR biosynthesis (Barrey et al, 2011;Murri and El Azzouzi, 2018;Kussainova et al, 2022). However, the verification of these mitomiRs as products of mitochondrial gene transcription remains elusive.…”

Section: Transportation Of Mirna Into Mitochondriamentioning

confidence: 88%

Mitochondrial-related microRNAs and their roles in cellular senescence

Luo,

An,

Xiao

et al. 2024

Front. Physiol.

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Aging is a natural aspect of mammalian life. Although cellular mortality is inevitable, various diseases can hasten the aging process, resulting in abnormal or premature senescence. As cells age, they experience distinctive morphological and biochemical shifts, compromising their functions. Research has illuminated that cellular senescence coincides with significant alterations in the microRNA (miRNA) expression profile. Notably, a subset of aging-associated miRNAs, originally encoded by nuclear DNA, relocate to mitochondria, manifesting a mitochondria-specific presence. Additionally, mitochondria themselves house miRNAs encoded by mitochondrial DNA (mtDNA). These mitochondria-residing miRNAs, collectively referred to as mitochondrial miRNAs (mitomiRs), have been shown to influence mtDNA transcription and protein synthesis, thereby impacting mitochondrial functionality and cellular behavior. Recent studies suggest that mitomiRs serve as critical sensors for cellular senescence, exerting control over mitochondrial homeostasis and influencing metabolic reprogramming, redox equilibrium, apoptosis, mitophagy, and calcium homeostasis-all processes intimately connected to senescence. This review synthesizes current findings on mitomiRs, their mitochondrial targets, and functions, while also exploring their involvement in cellular aging. Our goal is to shed light on the potential molecular mechanisms by which mitomiRs contribute to the aging process.

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Section: Transportation Of Mirna Into Mitochondriamentioning

confidence: 88%

Mitochondrial-related microRNAs and their roles in cellular senescence

Luo,

An,

Xiao

et al. 2024

Front. Physiol.

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“…Бұл бөлімді қорытындылай келе, әртүрлі микроРНҚ-лар митохондриялардың қызметтік белсенділігін реттеуде шешуші рөл атқаратынын атап өтуге болады [76,82]. Жасуша цитоплазмасында және митохондриялық матрицада митохондриялық ақуыздардың экспрессиясына қатысатын микроРНҚ-лар анықталды.…”

Section: митохондрияның функционалдық белсенділігіндегі микрорнқ-ның ...unclassified

Асбест Әсерінен Туындаған Өкпе Аурулары Жасушалық Механизмдеріндегі Митохондрияның Рөлі

Bersimbaev,

Ainagulova

2024

bulbioenu

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Mitochondria are one of the main sources of reactive oxygen species (ROS) and therefore they are actively involved in the regulation of cellular redox processes and ROS signalling. Mitochondrial dysfunction plays a critical role in bioenergy metabolism and the pathogenesis of many lung diseases. The processes of mitochondrial oxidative phosphorylation and their cellular functions are specific to different cells and tissues and can be heterogeneous even within a single cell due to the existence of subpopulations of mitochondria with distinct functional and structural properties. Mitochondrial function can change in response to changes in cellular metabolism. Damage to mitochondrial DNA (mtDNA) causes mitochondrial dysfunction, including disruption of the electron transport chain and loss of mitochondrial membrane potential. In addition, damaged mtDNA also acts as a damage-associated molecular pattern that triggers inflammatory and immune responses. Asbestos causes various lung diseases, the cellular and molecular mechanisms of which are not fully understood. Asbestos fibers can induce the production of mitochondrial ROS in lung epithelial cells and macrophages. This review article examines the molecular mechanisms of mitochondrial functioning when exposed to asbestos, as well as the formation and damage of mtDNA, reactive oxygen species, the effect of asbestos on ultrastructural changes in lung tissue mitochondria, and the role of microRNA in the functional activity of mitochondria.

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“…In a previous review, we discussed the extensive role of mitochondrial miRNAs in radon-induced lung cancer development, showing that prolonged radon exposure led to increased expression of miR-34a, miR-15a-5p, miR-19a-3p, and miR-21-5p and decreased levels of miR-144-5p, miR-193b-5p, and miR-32-3p [ 233 ].…”

Section: Radiation-induced Cellular Senescencementioning

confidence: 99%

The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation

Ibragimova,

Kussainova,

Aripova

et al. 2024

Cells

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This review discusses the relationship between cellular senescence and radiation exposure. Given the wide range of ionizing radiation sources encountered by people in professional and medical spheres, as well as the influence of natural background radiation, the question of the effect of radiation on biological processes, particularly on aging processes, remains highly relevant. The parallel relationship between natural and radiation-induced cellular senescence reveals the common aspects underlying these processes. Based on recent scientific data, the key points of the effects of ionizing radiation on cellular processes associated with aging, such as genome instability, mitochondrial dysfunction, altered expression of miRNAs, epigenetic profile, and manifestation of the senescence-associated secretory phenotype (SASP), are discussed. Unraveling the molecular mechanisms of cellular senescence can make a valuable contribution to the understanding of the molecular genetic basis of age-associated diseases in the context of environmental exposure.

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The Role of Mitochondrial miRNAs in the Development of Radon-Induced Lung Cancer

Cited by 11 publications

References 162 publications

Mitochondrial-related microRNAs and their roles in cellular senescence

Mitochondrial-related microRNAs and their roles in cellular senescence

Асбест Әсерінен Туындаған Өкпе Аурулары Жасушалық Механизмдеріндегі Митохондрияның Рөлі

The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation

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