TY - JOUR
T1 - Far-infrared irradiation restores mitochondrial dynamics to ameliorate ischemic stroke
AU - Wu, Wanyu
AU - Wang, Yuping
AU - Qin, Bo
AU - Xu, Xiongfei
AU - Qu, Yuanqing
AU - Wang, Nick
AU - Zheng, Wuyan
AU - Yun, Xiaoyun
AU - Law, Betty Yuen Kwan
AU - Sun, Jianfeng
AU - Zhang, Wei
AU - Chen, Chang
AU - Wong, Vincent Kam Wai
N1 - Publisher Copyright:
© 2026 Neural Regeneration Research.
PY - 2026/10/1
Y1 - 2026/10/1
N2 - Far-infrared irradiation exhibits promise in chronic diseases, and its role in ischemic stroke specifically in modulating mitochondrial dynamics remains unknown. This study explored the neuroprotective effects of far-infrared irradiation using a rat middle cerebral artery occlusion model and oxygen-glucose deprivation-injured neuronal cells. In middle cerebral artery occlusion rats, daily 30-minute far-infrared irradiation treatment reduced infarct volume, alleviated cerebral edema, and improved neurological function. Proteomic analysis identified far-infrared irradiation-mediated upregulation of eight proteins, including the mitochondrial fusion regulator optic atrophy 1. In oxygen-glucose deprivation-exposed cells, far-infrared irradiation restored mitochondrial membrane potential, and enhanced fusion via optic atrophy 1 induction. Mechanistically, far-infrared irradiation stabilized mitochondrial dynamics by boosting optic atrophy 1 expression, thereby reducing oxidative stress and maintaining energy production. Optic atrophy 1 knockdown partly abolished the protective effects of far-infrared irradiation therapy. These results establish far-infrared irradiation as a non-pharmacological intervention targeting mitochondrial redox homeostasis in ischemic stroke, offering a novel therapeutic avenue for cerebrovascular disorders.
AB - Far-infrared irradiation exhibits promise in chronic diseases, and its role in ischemic stroke specifically in modulating mitochondrial dynamics remains unknown. This study explored the neuroprotective effects of far-infrared irradiation using a rat middle cerebral artery occlusion model and oxygen-glucose deprivation-injured neuronal cells. In middle cerebral artery occlusion rats, daily 30-minute far-infrared irradiation treatment reduced infarct volume, alleviated cerebral edema, and improved neurological function. Proteomic analysis identified far-infrared irradiation-mediated upregulation of eight proteins, including the mitochondrial fusion regulator optic atrophy 1. In oxygen-glucose deprivation-exposed cells, far-infrared irradiation restored mitochondrial membrane potential, and enhanced fusion via optic atrophy 1 induction. Mechanistically, far-infrared irradiation stabilized mitochondrial dynamics by boosting optic atrophy 1 expression, thereby reducing oxidative stress and maintaining energy production. Optic atrophy 1 knockdown partly abolished the protective effects of far-infrared irradiation therapy. These results establish far-infrared irradiation as a non-pharmacological intervention targeting mitochondrial redox homeostasis in ischemic stroke, offering a novel therapeutic avenue for cerebrovascular disorders.
KW - energy metabolism
KW - far-infrared irradiation
KW - ischemic stroke
KW - middle cerebral artery occlusion (MCAO)
KW - mitochondrial dynamics
KW - mitochondrial fusion
KW - neuroprotection
KW - optic atrophy 1 (Opa1)
KW - oxidative stress
UR - https://www.scopus.com/pages/publications/105043733136
U2 - 10.4103/NRR.NRR-D-25-00399
DO - 10.4103/NRR.NRR-D-25-00399
M3 - Article
AN - SCOPUS:105043733136
SN - 1673-5374
VL - 21
SP - 4933
EP - 4944
JO - Neural Regeneration Research
JF - Neural Regeneration Research
IS - 10
ER -