bims-resufa Biomed News
on Respiratory supercomplex factors
Issue of 2026–10–04
two papers selected by
Gavin McStay, Liverpool John Moores University



  1. PLoS Pathog. 2026 Sep;22(9): e1014543
      Mitochondrial complexes, such as the mitochondrial electron transport chain (mETC), the F1Fo-ATP synthase, the mitochondrial ribosome and the Translocase of the Outer Membrane (TOM) complex are centrally important for mitochondrial function and cell survival. Recently, an unexpected diversity in the composition of these complexes across unicellular eukaryotic lineages, with the apicomplexan parasites featuring prominently, has been revealed. However, whether the observed enlarged and divergent mitochondrial complexes are conserved across the wider lineages has not been investigated. Here, using a complexome profiling proteomic approach, we have characterised the composition of the mitochondrial complexes of the myzozoan parasite of oysters, Perkinsus marinus. We show that it shares new components of ATP synthase and the mETC complexes that in the deadly apicomplexan Plasmodium and Toxoplasma were shown to be important for growth. Moreover, the Perkinsus mitoribosome possesses many of the divergent features recently discovered in apicomplexans, including members of the ApiAP2 family that until recently were all considered to be transcription factors. Our study reveals that the divergent subunit composition of mitochondrial complexes is an ancestral and highly conserved feature of Myzozoa.
    DOI:  https://doi.org/10.1371/journal.ppat.1014543
  2. Mitochondrion. 2026 Oct 01. pii: S1567-7249(26)00111-X. [Epub ahead of print] 102221
      Mitochondria and their biomacromolecular complexes-such as the electron transport chain (ETC), mitochondrial permeability transition pore (mPTP), and protein quality control systems-play pivotal roles in aging and age-related diseases. This review integrates recent insights into how structural and functional disruptions of these complexes drive cellular senescence and systemic decline. We outline the architecture of mitochondrial assemblies (e.g., oxidative phosphorylation (OXPHOS) complexes, mtDNA-protein interactions) essential for energy production and organelle stability. Age-related alterations in stoichiometry, conformational states (e.g., mPTP opening), and post-translational modifications (e.g., SIRT3-mediated acetylation) compromise mitochondrial integrity, fueling metabolic dysfunction and chronic inflammation ("inflammaging"). Therapeutic strategies include small-molecule stabilizers of ETC supercomplexes, peptide-based mPTP inhibitors, and CRISPR-mediated correction of mtDNA-protein mismatches. Tissue-specific models (e.g., Complex I in skin aging, Bcl-2 protein imbalance in ovarian aging) exemplify the clinical relevance. We also categorize nine age-associated diseases-neurodegenerative, cardiovascular, and cancer types-based on their dependence on distinct mitochondrial complexes, such as ATP synthase in cancer resistance and the TIM/TOM import machinery in Alzheimer's disease. By linking structural findings (e.g., cryo-EM studies) with therapeutic innovation, this review offers a framework for targeting mitochondrial complexes to mitigate aging and its related pathologies.
    Keywords:  Aging; Aging-related diseases; Mitochondria; Therapy; mtDNA
    DOI:  https://doi.org/10.1016/j.mito.2026.102221