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Peer-reviewedCC BY-NC-NDCell biology and toxicology

Mitochondrial remodeling with mitochondrial fusion promoter M1 for osteoarthritis therapy.

  • Xiangqian Zou1,2
  • Yibo Ma1
  • Zhi Yang1
  • Renjie Zhang1
  • Christine Tao1
  • Guohua Zhang3
  • Chenyue Xu4
  • Bingxin Liu5
  • Changjian Chen6
  • Liang Yang7
7 affiliations
  1. 1Department of Orthopedics, The Second Hospital of Dalian Medical University, Dalian, 116023, China.
  2. 2Department of Orthopedics, Dalian Third People's HospitalAffiliated to Dalian University of Technology, Dalian, 116033, China.
  3. 3Department of Orthopedics, Xi'an Qinhuang Hospital, Xi'an, 710000, China.
  4. 4School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
  5. 5Department of Orthopedics, The Second Hospital of Dalian Medical University, Dalian, 116023, China. [email protected].
  6. 6Department of Orthopedics, The Second Hospital of Dalian Medical University, Dalian, 116023, China. [email protected].
  7. 7Department of Orthopedics, The Second Hospital of Dalian Medical University, Dalian, 116023, China. [email protected].
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Abstract

Osteoarthritis (OA) is closely associated with mitochondrial dysfunction, but whether mitochondrial dynamics restoration can serve as an effective therapeutic entry point remains unclear. This study investigated the mitochondrial fusion promoter M1 (MFPM1) as a modulator of mitochondrial dynamics in OA and explored its target-associated mechanism. Bioinformatic and transcriptomic analyses linked OA progression and MFPM1 activity to mitochondrial dynamics, oxidative stress, inflammatory activation, apoptosis, and extracellular matrix (ECM) homeostasis. In OA-like chondrocytes, MFPM1 restored the balance between DNM1L/DRP1-associated fission signaling and MFN2/OPA1-associated fusion machinery, accompanied by recovery of mitochondrial energy metabolism and redox homeostasis and attenuation of inflammatory and apoptotic injury. Target prediction, molecular docking, molecular dynamics simulation, and CETSA identified GSK3B as a prioritized MFPM1 target, while GSK3B overexpression weakened the mitochondrial and cartilage-protective effects of MFPM1, supporting its functional involvement. MFPM1 further preserved ECM homeostasis and alleviated OA progression. These findings identify mitochondrial dynamics remodeling as a mechanistic entry point for OA intervention and support MFPM1 as a mitochondria-centered therapeutic candidate.

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Cite

BibTeXRIS
BibTeX
@article{zou2026mitochondrial,
  title = {{Mitochondrial remodeling with mitochondrial fusion promoter M1 for osteoarthritis therapy.}},
  author = {Xiangqian Zou and Yibo Ma and Zhi Yang and Renjie Zhang and Christine Tao and Guohua Zhang and Chenyue Xu and Bingxin Liu and Changjian Chen and Liang Yang},
  journal = {Cell biology and toxicology},
  year = {2026},
  month = aug,
  doi = {10.1007/s10565-026-10242-8},
  url = {https://europepmc.org/article/MED/42957931},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Mitochondrial remodeling with mitochondrial fusion promoter M1 for osteoarthritis therapy.
AU  - Xiangqian Zou
AU  - Yibo Ma
AU  - Zhi Yang
AU  - Renjie Zhang
AU  - Christine Tao
AU  - Guohua Zhang
AU  - Chenyue Xu
AU  - Bingxin Liu
AU  - Changjian Chen
AU  - Liang Yang
PY  - 2026
DA  - 2026/08/03
JO  - Cell biology and toxicology
DO  - 10.1007/s10565-026-10242-8
UR  - https://europepmc.org/article/MED/42957931
AB  - Osteoarthritis (OA) is closely associated with mitochondrial dysfunction, but whether mitochondrial dynamics restoration can serve as an effective therapeutic entry point remains unclear. This study investigated the mitochondrial fusion promoter M1 (MFPM1) as a modulator of mitochondrial dynamics in OA and explored its target-associated mechanism. Bioinformatic and transcriptomic analyses linked OA progression and MFPM1 activity to mitochondrial dynamics, oxidative stress, inflammatory activation, apoptosis, and extracellular matrix (ECM) homeostasis. In OA-like chondrocytes, MFPM1 restored the balance between DNM1L/DRP1-associated fission signaling and MFN2/OPA1-associated fusion machinery, accompanied by recovery of mitochondrial energy metabolism and redox homeostasis and attenuation of inflammatory and apoptotic injury. Target prediction, molecular docking, molecular dynamics simulation, and CETSA identified GSK3B as a prioritized MFPM1 target, while GSK3B overexpression weakened the mitochondrial and cartilage-protective effects of MFPM1, supporting its functional involvement. MFPM1 further preserved ECM homeostasis and alleviated OA progression. These findings identify mitochondrial dynamics remodeling as a mechanistic entry point for OA intervention and support MFPM1 as a mitochondria-centered therapeutic candidate.
SN  - 0742-2091
SN  - 1573-6822
ER  -