bims-cytox1 Biomed News
on Cytochrome oxidase subunit 1
Issue of 2026–03–01
two papers selected by
Gavin McStay, Liverpool John Moores University
  1. Integrative Proteomic and Bioenergetic Profiling Reveals Diet- and Strain-Specific Mitochondrial Dysfunction in Cohen Diabetic Rat Hearts.
  2. COX7A1-mediated mitochondrial dysfunction can induce ferroptosis in endometrial cancer cells.
  1. Antioxidants (Basel). 2026 Feb 13. pii: 248. [Epub ahead of print]15(2):
    Integrative Proteomic and Bioenergetic Profiling Reveals Diet- and Strain-Specific Mitochondrial Dysfunction in Cohen Diabetic Rat Hearts.
    Lauren Pavelich, Tasnim Arroum, Lucynda Pham, Dragana Komnenov, Paul M Stemmer, Rachel Lax, Ann Saada, Sarah Weksler-Zangen, Maik Hüttemann.
      Mitochondrial dysfunction contributes to diabetic cardiomyopathy, yet how genetic predisposition and diet interact to reshape cardiac metabolism in diabetic and prediabetic states remains unclear. The Cohen diabetic rat model, comprising diabetes-resistant (CDr) and diabetes-sensitive (CDs) strains, provides a unique platform to dissect this interplay. Here, we present an integrative global proteomic and bioenergetic characterization of cardiac tissue from CDr and CDs rats fed either a regular or a diabetogenic diet. Proteomic pathway mapping revealed downregulation of cytochrome c oxidase (CcO) subunits, strain-dependent rewiring of fatty-acid oxidation pathways, and CcO subunits switch from "heart-type" to "liver-type" isoforms in the sensitive strain. These changes were accompanied by impaired mitochondrial respiration, ATP depletion, and disruption of mitochondrial quality-control mechanisms, together with increased accumulation of tyrosine 304 phosphorylation of cytochrome c oxidase subunit I, indicative of inflammation-driven regulatory inhibition in a diet-specific manner. These findings establish an understanding of how genetic susceptibility and diet contribute to cardiac mitochondrial dysfunction in the Cohen diabetic rat model.
    Keywords:  CcO6A; CcO7A; cardiomyopathy; cytochrome c oxidase; heart mitochondria; mitochondrial dysfunction; mitochondrial quality control; phosphorylation; proteomic characterization; regulation; respiration; supercomplexes; type 2 diabetes; tyrosine 304 phosphorylation
    DOI:  https://doi.org/10.3390/antiox15020248
  2. PLoS One. 2026 ;21(2): e0342333
    COX7A1-mediated mitochondrial dysfunction can induce ferroptosis in endometrial cancer cells.
    Qi Wu, Suning Bai, Liyun Song, Lina Han, Pei Wang.
      In endometrial cancer, research on ferroptosis is still in its nascent stages, yet its potential therapeutic value is becoming increasingly evident. We explore the impact of COX7A1 on mitochondrial dysfunction and ferroptosis in endometrial cancer. In this study, through comprehensive bioinformatics analysis, differentially expressed genes related to ferroptosis in endometrial cancer were identified. In vitro experiments were conducted using cytochrome c oxidase subunit 7A1 (COX7A1) overexpression and knockdown cell lines, followed by ferroptosis-related phenotypic assays to validate the effect of COX7A1 on the inhibition of endometrial cancer cell growth. Mechanistically, mitochondrial function-related parameters were assessed to explore the potential mechanisms by which COX7A1 induces ferroptosis. Online data analysis revealed that COX7A1 acts as a ferroptosis driver and is significantly downregulated in endometrial cancer tissues. In vitro experiments have demonstrated that overexpression of COX7A1 inhibits the proliferation of endometrial cancer cells and induces ferroptosis by regulating intracellular iron metabolism and mitochondrial function. The specific mechanisms include increasing intracellular Fe2+ and malondialdehyde (MDA) levels, decreasing the GSH/GSSG ratio, and disrupting mitochondrial membrane potential, thereby leading to mitochondrial dysfunction. Furthermore, COX7A1 overexpression significantly reduces the expression of glutathione peroxidase 4 (GPX4) and SLC7A11, while upregulating acyl-coenzyme A synthetase long-chain family member 4 (ACSL4). In contrast, knockdown of COX7A1 promotes the proliferation of endometrial cancer cells and inhibits ferroptosis, exhibiting the opposite effects. These findings provide new insights into the molecular mechanisms of endometrial cancer.
    DOI:  https://doi.org/10.1371/journal.pone.0342333
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