ArticleCell death discovery2026
Cuproptosis causes meiotic metaphase I arrest by disrupting mitochondrial functions in oocytes.
Article in Cell death discovery, 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
Proper oocyte maturation is critical for female fertility, yet whether cuproptosis, a recently identified copper-dependent cell death pathway, affects meiotic maturation remains unknown. Here, we show that Cu(II)-elesclomol (ELC-Cu(II)) treatment induces dose-dependent metaphase I arrest of mouse oocytes. This arrest results from spindle assembly checkpoint activation caused by defective spindle organization and impaired kinetochore-microtubule attachments. We demonstrate that ELC-Cu(II) triggers changes in canonical cuproptosis markers, including intracellular copper accumulation, FDX1 downregulation, and protein aggregation. Meanwhile, treated oocytes exhibit mitochondrial dysfunction characterized by reduced membrane potential and decreased ATP levels. Integrated transcriptomic and proteomic profiling reveals a predominantly post-transcriptional response, with 223 differentially expressed proteins, while transcriptomic profiles show minimal changes. Pathway analysis identifies dysregulation of lipoic acid metabolism and iron-sulfur cluster biosynthesis as key features. Targeted knockdown of the key lipoyltransferase LIPT1 fails to rescue the meiotic defect, whereas supplementation with the NAD
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