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Mitochondrial Dysfunction Combined with Elevated CoQ10 Levels Specifically in Placental Cytotrophoblasts Suggests a Role for Mitophagy in Preeclampsia

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URI: http://hdl.handle.net/10498/39587

DOI: 10.3390/biology15020139

ISSN: 2079-7737

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Author/s
Abalos Martínez, Jessica; Visiedo García, Francisco ManuelAuthority UCA; Cascajo Almenara, María Victoria; Santos Rosendo, CelesteAuthority UCA; Melero Jiménez, VictoriaAuthority UCA; Santos Ocaña, Carlos; Vázquez Fonseca, LuisAuthority UCA; Bugatto González, FernandoAuthority UCA
Date
2026-01-13
Department
Anatomía y Embriología Humana; Biomedicina, Biotecnología y Salud Pública; Materno-Infantil y Radiología
Source
Biology. 2026 Jan 13;15(2):139
Abstract
Preeclampsia is a severe pregnancy disorder associated with significant morbidity and mortality for both the mother and the baby. The causes underlying the development of preeclampsia remain unknown, but it is well established that the placenta is the organ that triggers the disease and that its mitochondrial metabolism is compromised. This study suggests that the cytotrophoblast is a placental cell type that is particularly affected at the mitochondrial level in preeclampsia. This mitochondrial dysfunction observed in this cell type is accompanied by an increase in coenzyme Q10 levels, which may represent a compensatory response. The data also suggest the activation of a second potential adaptive mechanism in cytotrophoblasts in response to mitochondrial dysfunction—mitophagy. This alteration and putative compensatory response were not observed in syncytiotrophoblasts. These findings highlight the possible specific involvement of the cytotrophoblast during preeclampsia, a cell type characterized by high mitochondrial activity within the placenta. Overall, these observations support the relevance of cytotrophoblast mitochondrial metabolism for future mechanistic studies aimed at better understanding preeclampsia.
Subjects
preeclampsia; mitochondria; cytotrophoblast; mitophagy; coenzyme Q10
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Attribution 4.0 Internacional
This work is under a Creative Commons License Attribution 4.0 Internacional

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