Morphological markers of mitochondrial dysfunction of the basal plate cytotrophoblast of the placenta in preeclampsia of varying severity

Khizrieva Z.S.; Kulida L.V.; Panova I.A.

doi:https://doi.org/10.17116/patol20258702124

Khizrieva Z.S.

Ivanovo Scientific Research Institute of Motherhood and Childhood named after V.N. Gorodkov

ORCID: 0009-0006-0192-7678

Kulida L.V.

Scientific Research Institute of Motherhood and Childhood named after V.N. Gorodkov

SPIN RSCI: 6208-4487
Scopus AuthorID: 7801518458
ResearcherID: B-1080-2017
ORCID: 0000-0001-8962-9048

Panova I.A.

Ivanovo Scientific Research Institute of Motherhood and Childhood named after V.N. Gorodkov

ORCID: 0000-0002-1145-0563

Morphological markers of mitochondrial dysfunction of the basal plate cytotrophoblast of the placenta in preeclampsia of varying severity

Authors:

Khizrieva Z.S., Kulida L.V., Panova I.A.

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Journal: Russian Journal of Archive of Pathology. 2025;87(2): 24‑29

DOI: 10.17116/patol20258702124

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To cite this article:

Khizrieva ZS, Kulida LV, Panova IA. Morphological markers of mitochondrial dysfunction of the basal plate cytotrophoblast of the placenta in preeclampsia of varying severity. Russian Journal of Archive of Pathology. 2025;87(2):24‑29. (In Russ.)
https://doi.org/10.17116/patol20258702124

Подписка 2026 Архив патологии (Russian Journal of Archive of Pathology)

Использование инфографики авторами научных работ

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OBJECTIVE

To identify morphological markers of mitochondrial dysfunction of the basal plate cytotrophoblast of the placenta in women with preeclampsia of varying severity.

MATERIAL AND METHODS

Comprehensive morphological examination of placentas from women with uncomplicated pregnancy (30), moderate (30) and severe (30) preeclampsia included overview histology, morphometry, immunohistochemistry and transmission electron microscopy.

RESULTS

Regardless of the severity of preeclampsia, a leading place in the pathomorphological change in the placenta is occupied by a violation of uteroplacental circulation due to a violation of cytotrophoblast invasion. Immunohistochemical parameters of mitochondrial dysfunction of cytotrophoblast cells of the basal lamina have been determined. A significant decrease in the expression of mtDNA transcription and replication proteins (TFAM, POLG) and a violation of the structure of the respiratory chain (NADH+, cytochrome C) were revealed. These changes were combined with ultrastructural rearrangement of mitochondria, which are the basis of ATP synthesis. In moderate preeclampsia, a decrease in the number of mitochondria was revealed, the ratio of oval and rounded forms of mitochondria associated with swelling of the central parts of the crist changes. In severe preeclampsia, the structural basis of the connection of energy metabolism between mitochondria and the granular endoplasmic reticulum is interrupted. The progressive destruction of mitochondrial crysts with the formation of pseudovesicles ends with total necrosis of ultrastructures.

CONCLUSION

In pregnant women with preeclampsia, mitochondrial dysfunction of the cytotrophoblast cells of the basal lamina was diagnosed, characterized by a decrease in the expression of mtDNA transcription and replication proteins in combination with a violation of the I–III enzymatic complexes of the respiratory chain. The identified immunohistochemical markers are pathogenetically associated with ultrastructural rearrangement of mitochondria in preeclampsia of varying severity.

Keywords:

preeclampsia

cytotrophoblast

mitochondrial dysfunction

respiratory chain

TEAM

POLG

cytochrome C

Authors:

Khizrieva Z.S.

Ivanovo Scientific Research Institute of Motherhood and Childhood named after V.N. Gorodkov

ORCID: 0009-0006-0192-7678

Kulida L.V.

Scientific Research Institute of Motherhood and Childhood named after V.N. Gorodkov

SPIN RSCI: 6208-4487
Scopus AuthorID: 7801518458
ResearcherID: B-1080-2017
ORCID: 0000-0001-8962-9048

Panova I.A.

Ivanovo Scientific Research Institute of Motherhood and Childhood named after V.N. Gorodkov

ORCID: 0000-0002-1145-0563

Received:

01.07.2024

Accepted:

18.12.2024

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