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Peer-reviewedCC BY-NC-ND 4.0Bioactive Materials

Mitochondria-rich cytochalasomes as an intravenously deliverable vesicle platform for ischemic heart disease

  • Xiong Gao1,2,3,4,5
  • Lu Zhang1,2,3,4,5,6,7,8
  • Lei Xu1,2,3,4,5
  • Yawei Jin1,2,3,4,5
  • Benheng Qian1,2,3,4,5
  • Yuning Zhang1,2,3,4,5
  • Mohan Li1,2,3,4,5
  • Ze Yuan1,2,3,4,5
  • Yihua Lu1,2,3,4,5
  • Nan Qiu1,2,3,4,5
  • Peng Wang1,2,3,4,5
  • Xiaolei Sun1,2,3,4,5
2 more authors
  • Junbo Ge1,2,3,4,5,9
  • Aijun Sun1,2,3,4,5,9,10
10 affiliations
  1. 1Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Qidong-Fudan Innovative Institute of Medical Sciences, China.
  2. 2State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, China.
  3. 3NHC Key Laboratory of Ischemic Heart Diseases, China.
  4. 4Key Laboratory of Viral Heart Diseases, Chinese Academy of Medical Sciences, China.
  5. 5National Clinical Research Center for Interventional Medicine, Shanghai, China.
  6. 6Shanxi Medical University, Taiyuan, Shanxi Province, China.
  7. 7Second Hospital of Shanxi Medical University, Taiyuan, Shanxi Province, China.
  8. 8Oriental Pan-vascular Devices Innovation College, University of Shanghai for Science and Technology, Shanghai, China.
  9. 9Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
  10. 10Zhengzhou Seventh People's Hospital, Zhengzhou, Henan Province, China.
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Abstract

Poor organelle viability and rapid immune clearance limit mitochondrial transplantation for ischemic disease. Here, we engineer mitochondria-rich cytochalasomes (MRCs) as an intravenously deliverable vesicle platform. MRCs are generated through cytoskeletal remodeling in mesenchymal stem cells. They encapsulate functional mitochondria, protecting them from extracellular stressors and inheriting immunomodulatory proteins, which reduce macrophage phagocytosis by more than sixfold. Mechanistically, MRCs do not fuse with the host mitochondrial network but instead are trafficked to lysosomes and trigger protective autophagy-lysosomal response. In a murine myocardial ischemia/reperfusion (I/R) model, a single intravenous injection of MRCs reduced infarct size by 52% and preserved cardiac function for up to 28 days, whereas isolated mitochondria were ineffective. This work positions MRCs as a promising intravenously deliverable vesicle platform for ischemic heart disease and reveals a non-fusogenic mechanism.

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Cite

BibTeXRIS
BibTeX
@article{gao2026mitochondriarich,
  title = {{Mitochondria-rich cytochalasomes as an intravenously deliverable vesicle platform for ischemic heart disease}},
  author = {Xiong Gao and Lu Zhang and Lei Xu and Yawei Jin and Benheng Qian and Yuning Zhang and Mohan Li and Ze Yuan and Yihua Lu and Nan Qiu and Peng Wang and Xiaolei Sun and Junbo Ge and Aijun Sun},
  journal = {Bioactive Materials},
  year = {2026},
  month = oct,
  doi = {10.1016/j.bioactmat.2026.09.036},
  url = {https://doi.org/10.1016/j.bioactmat.2026.09.036},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Mitochondria-rich cytochalasomes as an intravenously deliverable vesicle platform for ischemic heart disease
AU  - Xiong Gao
AU  - Lu Zhang
AU  - Lei Xu
AU  - Yawei Jin
AU  - Benheng Qian
AU  - Yuning Zhang
AU  - Mohan Li
AU  - Ze Yuan
AU  - Yihua Lu
AU  - Nan Qiu
AU  - Peng Wang
AU  - Xiaolei Sun
AU  - Junbo Ge
AU  - Aijun Sun
PY  - 2026
DA  - 2026/10/17
JO  - Bioactive Materials
DO  - 10.1016/j.bioactmat.2026.09.036
UR  - https://doi.org/10.1016/j.bioactmat.2026.09.036
AB  - Poor organelle viability and rapid immune clearance limit mitochondrial transplantation for ischemic disease. Here, we engineer mitochondria-rich cytochalasomes (MRCs) as an intravenously deliverable vesicle platform. MRCs are generated through cytoskeletal remodeling in mesenchymal stem cells. They encapsulate functional mitochondria, protecting them from extracellular stressors and inheriting immunomodulatory proteins, which reduce macrophage phagocytosis by more than sixfold. Mechanistically, MRCs do not fuse with the host mitochondrial network but instead are trafficked to lysosomes and trigger protective autophagy-lysosomal response. In a murine myocardial ischemia/reperfusion (I/R) model, a single intravenous injection of MRCs reduced infarct size by 52% and preserved cardiac function for up to 28 days, whereas isolated mitochondria were ineffective. This work positions MRCs as a promising intravenously deliverable vesicle platform for ischemic heart disease and reveals a non-fusogenic mechanism.
SN  - 2452-199X
ER  -