ArticleFrontiers in cell and developmental biology2026
Coq4 deficiency induces placental vascular development defects through FSP1/CoQ10 axis-mediated endothelial ferroptosis.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Coenzyme Q10 (CoQ10), a critical electron carrier in mitochondrial respiratory chains, is essential for cellular energy metabolism. Ubiquinone biosynthesis protein 4 homolog (Coq4), a rate-limiting enzyme in CoQ10 biosynthesis, is indispensable for embryonic development. However, the mechanisms underlying Coq4 deficiency-induced developmental defects remain elusive. Emerging evidence highlights the FSP1/CoQ10 axis as a central regulator of lipid peroxidation and ferroptosis, a non-apoptotic cell death mechanism implicated in placental vascular dysgenesis and trophoblast dysfunction. This study aims to elucidate the molecular mechanisms by which Coq4 deficiency disrupts placental development, with a focus on the interplay between the FSP1/CoQ10 axis and endothelial ferroptosis. Methods: Coq4 Results: Coq4 Discussion: This study demonstrates that Coq4 deficiency induces endothelial ferroptosis via disrupting the FSP1-CoQ10 antioxidant axis, and may also provide new insights into the pathogenesis of pregnancy complications caused by placental dysfunction and iron-related vascular diseases, while offering novel approaches for exploring potential therapeutic targets.
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