Journal of shoulder and elbow surgery · 2025
Platelet-derived mitochondria attenuate muscle atrophy following rotator cuff tears in a rat model.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Xin, Gao Xing, Deng Chunchu, Xu Ding, Chen Yuanyuan, Huang Jiaqi, Li Xiao, Shi Yulong
Аннотация
BACKGROUND: Rotator cuff tears (RCTs) often result in muscle atrophy, compromising surgical outcomes and recovery. Mitochondrial dysfunction is implicated in this process, suggesting potential for mitochondria-based therapies. This study aimed to investigate the effects of platelet-derived mitochondria (Plt-Mito) administration into the supraspinatus muscle (SSP) following RCTs.
METHODS: Seventy-two male Sprague-Dawley rats were allocated into 3 distinct groups: (1) a sham surgery group, (2) a group with RCTs treated with Plt-Mito, and (3) a group with RCTs treated with phosphate-buffered saline. Treatments were administered every 2 weeks. After 12 weeks, the SSPs were analyzed for wet muscle weight ratio, muscle fiber cross-sectional area, fibrosis, antioxidant activity, mitochondrial markers, capillary density, and mitochondrial structure.
RESULTS: Plt-Mito successfully incorporated into SSP, maintaining functional integrity. Compared to the phosphate-buffered saline group, Plt-Mito treatment significantly preserved wet muscle weight, increased mean muscle fiber cross-sectional area, promoted muscle regeneration, reduced fibrosis, enhanced antioxidant activity (increased superoxide dismutase activity and decreased malondialdehyde activity), improved muscle vascularity (increased platelet endothelial cell adhesion molecule-1 and α-smooth muscle actin), increased expression of mitochondrial markers (C oxidase subunit IV and uncoupling protein 1) and maintained mitochondrial density and structure.
CONCLUSIONS: Our findings demonstrated Plt-Mito administration effectively halted muscle atrophy and fibrosis, while attenuating mitochondrial damage and dysfunction following RCTs.
METHODS: Seventy-two male Sprague-Dawley rats were allocated into 3 distinct groups: (1) a sham surgery group, (2) a group with RCTs treated with Plt-Mito, and (3) a group with RCTs treated with phosphate-buffered saline. Treatments were administered every 2 weeks. After 12 weeks, the SSPs were analyzed for wet muscle weight ratio, muscle fiber cross-sectional area, fibrosis, antioxidant activity, mitochondrial markers, capillary density, and mitochondrial structure.
RESULTS: Plt-Mito successfully incorporated into SSP, maintaining functional integrity. Compared to the phosphate-buffered saline group, Plt-Mito treatment significantly preserved wet muscle weight, increased mean muscle fiber cross-sectional area, promoted muscle regeneration, reduced fibrosis, enhanced antioxidant activity (increased superoxide dismutase activity and decreased malondialdehyde activity), improved muscle vascularity (increased platelet endothelial cell adhesion molecule-1 and α-smooth muscle actin), increased expression of mitochondrial markers (C oxidase subunit IV and uncoupling protein 1) and maintained mitochondrial density and structure.
CONCLUSIONS: Our findings demonstrated Plt-Mito administration effectively halted muscle atrophy and fibrosis, while attenuating mitochondrial damage and dysfunction following RCTs.