bims-humivi Biomed News
on Human mito-nuclear genetic interplay
Issue of 2025–09–28
two papers selected by
Mariangela Santorsola, Università di Pavia
  1. From Ancient Philosophy to Endosymbiotic Theory: The Bacterial Origin and Key Role of Mitochondria in Immune Responses.
  2. The Emerging Role of Mitochondrial Dysfunction in Thyroid Cancer: Mediating Tumor Progression, Drug Resistance, and Reshaping of the Immune Microenvironment.
  1. Microorganisms. 2025 Sep 15. pii: 2149. [Epub ahead of print]13(9):
    From Ancient Philosophy to Endosymbiotic Theory: The Bacterial Origin and Key Role of Mitochondria in Immune Responses.
    Alexandra Mpakosi, Christiana Kaliouli-Antonopoulou, Vasileios Cholevas, Stamatios Cholevas, Ioannis Tzouvelekis, Maria Mironidou-Tzouveleki, Emmanuel A Tsantes, Deny Tsakri, Marianna Vlachaki, Stella Baliou, Petros Ioannou, Rozeta Sokou, Stefanos Bonovas, Andreas G Tsantes.
      The endosymbiotic theory, which is the crucial starting point of eukaryogenesis, was first mentioned in the philosophy of the pre-Socratic Greek philosopher Empedocles. According to him, everything merges into units with differential survival. Similarly, during eukaryogenesis, the fusion of two distinct units resulted in the creation of a new cell type that possessed a newly formed organelle, the mitochondrion. Since then, the mitochondrion has been a key regulator of health and immunity. Furthermore, many of its characteristics and functions are due to its endosymbiotic bacterial origin. For example, it possesses damage-associated molecular patterns that can activate inflammatory signaling pathways, has circular DNA with CpG-rich motifs, as well as a double phospholipid membrane, and divides by fission. Mitochondrial function plays a critical role in maintaining cellular homeostasis, as they meet the cell's energy needs and regulate many of its functions. However, after cellular damage due to infection, radiation, or toxins, mitochondrial stress and dysfunction can occur and mitochondrial DNA can be released into the cytosol. Cytosolic mitochondrial DNA can then activate proinflammatory signaling pathways, mediated by TLR9 and cGAS, as well as inflammasomes, triggering inflammation and autoimmunity.
    Keywords:  cellular homeostasis; endosymbiosis; eukaryotic cell; evolution; immune responses; inflammasome; mitochondrial DNA; proinflammatory signaling pathways
    DOI:  https://doi.org/10.3390/microorganisms13092149
  2. Biomolecules. 2025 Sep 08. pii: 1292. [Epub ahead of print]15(9):
    The Emerging Role of Mitochondrial Dysfunction in Thyroid Cancer: Mediating Tumor Progression, Drug Resistance, and Reshaping of the Immune Microenvironment.
    Yating Zhang, Hengtong Han, Tingting Zhang, Tianying Zhang, Libin Ma, Ze Yang, Yongxun Zhao.
      As the hub of energy metabolism and the cell's fate arbiter, mitochondria are essential for preserving cellular homeostasis and converting it from pathological states. Therefore, through mechanisms that drive metabolic reprogramming, oxidative stress, and apoptosis resistance, mitochondrial dysfunction (including mitochondrial DNA mutations, mitochondrial dynamics imbalance, mitochondrial autophagy abnormalities, mitochondrial permeability abnormalities, and metabolic disorder) can promote the progression of thyroid cancer (TC), resistance to treatment, and reshaping of the immune microenvironment. This article reviews the molecular mechanisms and characteristic manifestations of mitochondrial dysfunction in TC. It focuses on providing a summary of the main strategies currently used to target the mitochondria, such as dietary intervention and targeted medications like curcumin, as well as the clinical translational value of these medications when used in conjunction with current targeted therapies for TC and radioactive iodine (RAI) therapy in patients with advanced or RAI-refractory TC who rely on targeted therapies. The application prospects and existing challenges of emerging therapeutic methods, such as mitochondrial transplantation, are also discussed in depth, aiming to provide new perspectives for revealing the molecular mechanisms by which mitochondrial dysfunction drives the progression of TC, drug resistance, and the reshaping of its immune microenvironment, as well as providing new diagnostic and therapeutic strategies for patients with advanced or RAI-refractory TC who are reliant on targeted therapies.
    Keywords:  mitochondria; mitochondrial autophagy; mitochondrial dynamics; mitochondrial metabolism; thyroid cancer
    DOI:  https://doi.org/10.3390/biom15091292
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