bims-mithem Biomed News
on Mitochondria in Hematopoiesis
Issue of 2026–10–04
two papers selected by
Tim van Tienhoven, Erasmus Medical Center
  1. Adult hematopoietic stem cells activate a normally fetal-restricted program to functionally expand ex vivo.
  2. Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.
  1. Blood. 2026 Nov 04. pii: blood.2025030268. [Epub ahead of print]
    Adult hematopoietic stem cells activate a normally fetal-restricted program to functionally expand ex vivo.
    Kyomi J Igarashi, Matthew Nicholls, Leonid Olender, Apapist Panichewa, Toshiya Nishimura, Paul K Mack, Shady Saad, Wesley Huang, Alia Mn Welsh, Dean C Pask, Ryo Yamamoto, Stefan A Muljo, Hiromitsu Nakauchi, Adam C Wilkinson.
      The ability to robustly expand transplantable hematopoietic stem cells (HSCs) ex vivo enables basic science and clinical therapies otherwise hindered by the scarcity of these self-renewing multipotent cells. Despite recent improvements in long-term ex vivo HSC expansion conditions, the molecular mechanisms required for successful ex vivo expansion of functional HSCs remain unknown. Here we characterized the ex vivo expansion potential of HSCs from mouse fetal liver, young bone marrow, and aged bone marrow at the functional and molecular levels. We find that Lin28b, the in vivo fetal-restricted gene, contributes to the mechanism of both fetal and adult ex vivo HSC expansion. The expression of Lin28b correlates with reconstitution potential, with higher levels observed in HSCs expanded from the fetal liver and young adults. By contrast, expanded aged HSCs fail to robustly express Lin28b and also fail to stably reconstitute the hematopoietic system following transplantation. Consistent with a functional role for this fetal program in ex vivo expanded HSCs, Lin28b-deficient HSCs display aging-associated molecular and functional features following ex vivo expansion cultures. Importantly, Lin28b overexpression during ex vivo expansion was sufficient to enhance reconstitution potential of aged HSCs. In summary, we identify Lin28b as an important regulator of functional HSC expansion ex vivo, suggesting novel opportunities for HSC rejuvenation and clinical applications.
    DOI:  https://doi.org/10.1182/blood.2025030268
  2. Geroscience. 2026 Sep 28.
    Therapeutic potential of MitoQ, a mitochondria-targeted antioxidant, in age-related physiological dysfunction.
    Siyun Kim, Sung Gi Noh, Minje Ji, Kai Chen, George A Kuchel, Iman M Al-Naggar, Oh Sung Kwon.
      Aging is an inevitable and progressive physiological process marked by a decline in cellular function, accumulation of somatic mutations, decreased ability to maintain homeostasis, and increased tissue and organ dysfunction. These changes contribute to the onset and progression of various age-related diseases. Accumulation of reactive oxygen species (ROS) has been identified as a key mediator of the aging process. Mitochondria, the primary producers of ROS, accumulate defects with aging, leading to increased mitochondrial oxidative stress. These defective mitochondria are both a source and a target of oxidative stress, creating a vicious cycle that accelerates aging and the progression of age-related diseases. Consequently, targeting mitochondria represents a promising therapeutic approach to prevent aging-related physiological dysfunction. MitoQ, a mitochondria-targeted antioxidant, has been extensively studied due to its ability to effectively scavenge mitochondria-derived ROS, owing to its lipophilic cation properties. This review explores the effects of MitoQ on aging-associated physiological dysfunction, specifically exploring its impact on cardiovascular, neuronal, and skeletal muscle functions. By addressing the central role of mitochondrial oxidative stress, we propose that MitoQ represents a promising strategy to counteract aging-associated physiological dysfunction.
    Keywords:  Age-related disease; Aging; MitoQ; Mitochondria-derived ROS; Mitochondria-targeted antioxidants; Oxidative stress
    DOI:  https://doi.org/10.1007/s11357-026-02515-1
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