bims-mitrat Biomed News
on Mitochondrial transplantation and transfer
Issue of 2025–05–11
two papers selected by
Gökhan Burçin Kubat, Gulhane Health Sciences Institute
  1. Targeting mitochondrial transfer as a promising therapeutic strategy.
  2. Neuronal FGF13 Inhibits Mitochondria-Derived Damage Signals to Prevent Neuroinflammation and Neurodegeneration in a Mouse Model of Parkinson's Disease.
  1. Trends Mol Med. 2025 May 06. pii: S1471-4914(25)00089-9. [Epub ahead of print]
    Targeting mitochondrial transfer as a promising therapeutic strategy.
    Bo Li, Bingzhi Li, Xianghe Qiao, Wanrong Meng, Yuhang Xie, Jiajing Gong, Yi Fan, Zhihe Zhao, Longjiang Li.
      Despite the primary impression of mitochondria as energy factories, these organelles are increasingly recognized for their multifaceted roles beyond energy production. Intriguingly, mitochondria can transfer between cells, influencing physiological and pathological processes through intercellular trafficking termed 'mitochondrial transfer.' This phenomenon is important in maintaining metabolic homeostasis, enhancing tissue regeneration, exacerbating cancer progression, and facilitating immune modulation, depending on the cell type and microenvironment. Recently, mitochondrial transfer has emerged as a promising therapeutic target for tissue repair and antitumor therapy. Here, we summarize and critically review recent advances in this field. We aim to provide an updated overview of the mechanisms and potential therapeutic avenues associated with mitochondrial transfer in various diseases from the perspective of different donor cells.
    Keywords:  cancer; immunity; mesenchymal stem/stromal cells MSCs; mitochondrial transfer; regeneration
    DOI:  https://doi.org/10.1016/j.molmed.2025.04.002
  2. Adv Sci (Weinh). 2025 May 08. e2503579
    Neuronal FGF13 Inhibits Mitochondria-Derived Damage Signals to Prevent Neuroinflammation and Neurodegeneration in a Mouse Model of Parkinson's Disease.
    Nanshan Song, Xiangxu Wang, Luqing Ha, Lamei Hu, Shuyuan Mei, Yue Liang, Yujie Zhao, Xingyin Yang, Qingyu Zhang, Yuanzhang Zhou, Jianhua Ding, Yan Liu, Qigang Zhou, Feng Han, Gang Hu, Ming Lu.
      Fibroblast growth factor homologous factors (FHFs) are highly expressed in the central nervous system (CNS). It is demonstrated that the FHFs subfamily plays cardinal roles in several neuropathological diseases, while their involvement in Parkinson's disease (PD) has been so far scarcely investigated. From the publicly available Gene Expression Omnibus (GEO) datasets, FHF2 (also known as fibroblast growth factor 13, FGF13) alterations are described in PD patients. Fgf13 gene is significantly decreased in several PD mouse models, and its overexpression alleviates the PD-like pathological phenotype. Although FGF13 is highly expressed in neurons, it functions by preventing glia-dependent inflammatory processes. Mechanistically, FGF13 combines mitochondrial proteins such as MCHT2 (a protein localized on the mitochondrial outer membrane), to anchor mitochondria within the cytoplasm. Under PD-related stress, decreased neuronal FGF13 levels induce the release of the damaged mitochondria, which in turn activate microglia and astrocytes, thereby promoting neurodegeneration. Abacavir, an FDA-applied anti-retroviral drug, is identified to prevent excessive gliosis and neuron loss in both glia-neuron co-cultures and PD mouse models by rejuvenating FGF13 signaling. Collectively, neuronal FGF13 inhibits the transfer of stressed mitochondria to glia, thereby impeding neuroinflammation and neurodegeneration. Abacavir is a promising neuroprotectant and sets a brake to PD progression.
    Keywords:  FGF13; MTCH2; mitochondrial transfer; neuroinflammation; parkinson's disease
    DOI:  https://doi.org/10.1002/advs.202503579
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