Role of mitochondrial dysfunction in the pathogenesis of premature birth
The pathophysiology of premature birth remains insufficiently studied. One of the mechanisms of is development is considered to be mitochondrial dysfunction and an imbalance between increased oxidative stress and impaired antioxidant protection. At the molecular level, the changed and impaired mitochondrial function is caused by a reduction in the metachondrial transfer of major metabolites; by a change or a loss in maintaining the electric and chemical transmembrane potential of the inner mitochondrial membrane. In consequence of these modifications, oxidative phosphorylation becomes less effective, accordingly causes a reduction in ATP production. The division and creation of new mitochondria, митохондрий, the removal and complete degradation of dysfunctional mitochondria (mitophagia) can affect the function of the placenta, including its development, nutrient exchange and hormonal release. The modifications of mitochondrial function may be mediated or may lower the impact of poor gestational conditions on placental function, therefore the risk of pregnancy complications, including premature birth.Medzhidova M.K., Tyutyunnik V.L., Kan N.Е., Vysokikh M.Yu.
Conclusion: Identification of molecular pathways responsible for the elimination of dysfunctional mitochondrial may play a key role and be one of the components of the pathogenesis of premature birth.
Authors' contributions: Medzhidova M.K., Tyutyunnik V.L., Kan N.Е., Vysokikh M.Yu. – concept and development of the design of the investigation, obtaining the data to be analyzed, collection of publications, processing and analysis of material on the topic, writing the text of the manuscript, editing the article.
Conflicts of interest: The authors declare that there are no conflicts of interest.
Funding: The investigation has not been sponsored.
For citation: Medzhidova M.K., Tyutyunnik V.L., Kan N.Е., Vysokikh M.Yu. Role of mitochondrial dysfunction in the pathogenesis of premature birth. Akusherstvo i Ginekologiya/Obstetrics and Gynecology. 2023; (5): 5-11 (in Russian)
https://dx.doi.org/10.18565/aig.2023.31
Keywords
premature birth
mitochondrial dysfunction
oxidative stress
antioxidative protection
mitochondrial DNA
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Received 24.01.2023
Accepted 28.04.2023
About the Authors
Marzhanat К. Medzhidova, PhD, Doctoral student, Academician V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Ministry of Health of Russia, +7(926)381-17-10, Researcher ID: GRR-7195-2022, SPIN-код: 5942-2320, Authors ID: 1162986, Scopus Author ID: 57191960453, https://orcid.org/0000-0001-6938-4207, 117997, Russia, Moscow, Ac. Oparina str., 4.Victor L. Tyutyunnik, Professor, MD, PhD, Leading Researcher of Research and Development Service, Academician V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Ministry of Health of Russia, +7(903)969-50-41, tioutiounnik@mail.ru, Researcher ID: B-2364-2015, SPIN-код: 1963-1359, Authors ID: 213217, Scopus Author ID: 56190621500, https://orcid.org/0000-0002-5830-5099, 117997, Russia, Moscow, Ac. Oparina str., 4.
Natalia E. Kan, Professor, MD, PhD, Deputy Director of Science, Academician V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Ministry of Health of Russia, +7(926)220-86-55, kan-med@mail.ru, Researcher ID: B-2370-2015, SPIN-код: 5378-8437, Authors ID: 624900, Scopus Author ID: 57008835600, https://orcid.org/0000-0001-5087-5946, 117997, Russia, Moscow, Ac. Oparina str., 4.
Mikhail Yu. Vysokikh, PhD, Head of Mitochondrial Medicine Research Group, Academician V.I. Kulakov National Medical Research Center for Obstetrics, Gynecology and Perinatology, Ministry of Health of the Russia, +7(495)438-76-33 (доб. 1472), m_vysokikh@oparina4.ru, Researcher ID: H-4744-2014, SPIN-код: 2742-0833, Authors ID: 6602218584, Scopus Author ID: 57008835600, https://orcid.org/0000-0002-4047-6201, 117997, Russia, Moscow, Ac. Oparina str., 4.
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