News Express: UM research team proposes new approach to treating muscle atrophy
jasonleong2025-04-01T15:17:39+08:00
研究發現,在飢餓或衰老誘導的肌肉萎縮中,肌肉細胞不會因細胞凋亡而死亡,而是通過自噬保持存活
The study shows that in starvation or aging-induced muscle atrophy, muscle cells do not die by apoptosis but remain alive through autophagy
澳大提出治療肌肉萎縮新方法
澳門大學健康科學學院教授羅茜帶領的團隊建立了基於熒光探針斑馬魚的肌肉萎縮新模型。研究顯示萎縮的肌肉可以通過增加單個肌肉細胞的大小來提高整體肌肉的體積和力量,最終改善患者的行動能力和健康狀況,為治療肌肉萎縮提供了新的見解和思路。相關研究成果已發表在國際知名期刊《先進科學》(Advanced Science)。
在衰老、長期臥床、飢餓、神經損傷、腫瘤等疾病的情況下,人體的肌肉會發生萎縮,從而導致行動能力的下降。在過去的幾十年中,人們使用了許多種方法來治療肌肉萎縮,包括運動、電刺激、超音波治療、營養治療等。然而,這些方法的效果並不令人滿意。在肌肉萎縮過程中,肌肉體積變小可能是由於肌肉細胞的死亡或是因為單個肌細胞變小所致。因此,弄清這個問題對於治療因肌肉萎縮造成的各種疾病和改善健康狀況至關重要。
為了準確檢測肌肉細胞的凋亡,研究團隊建立了一種在活體斑馬魚體內實時測定肌肉細胞凋亡的方法。團隊將一種基因編碼的蛋白熒光探針特異性地表達在斑馬魚的肌肉組織中,該探針在活細胞中發出綠色熒光,而在凋亡細胞中發出藍色熒光。團隊發現在饑餓誘導的肌肉萎縮中,斑馬魚肌肉細胞雖然明顯變小,但並未發生凋亡。這些萎縮的肌肉細胞通過吞噬自身的細胞組分來保持存活,也就是自噬。對發生肌肉萎縮的斑馬魚重新進行餵養後,自噬現象便會消失,意味着肌肉萎縮是可以被恢復的。
一般而言,斑馬魚的壽命為三到五年。為了研究因衰老導致的肌肉萎縮,團隊對熒光探針的斑馬魚進行了長達五年的跟蹤。他們發現在肌肉萎縮的斑馬魚中,儘管肌肉細胞的直徑減少了57%,這些肌肉細胞依舊保持存活。通過檢測基因轉錄水平,他們發現與凋亡相關的基因表達明顯下調;相反,多種和自噬相關的基因表達顯著上調。
是次研究發現在飢餓和衰老引起的肌肉萎縮中,肌肉細胞沒有死亡,並通過自噬來維持其生命。研究亦提示,對於萎縮的肌肉可以通過增加單個肌肉細胞的大小來提高整體肌肉的體積和力量,最終改善患者的行動能力和健康狀況。
羅茜為是次研究的通訊作者,澳大健康科學學院博士後賈皓為第一作者,博士畢業生吳仁飛和楊紅梅也參與了相關研究工作。澳大健康科學學院動物研究核心實驗中心和生物成像及幹細胞核心實驗中心提供了重要支援。研究的資助來自澳門大學(檔案編號:MYRG2020-00121-FHS、MYRG2022-00025-FHS),澳門特別行政區科學技術發展基金(檔案編號:0147/2020/A3、044/2021/APD、0004/2021/AKP)和國家教育部澳門大學精準腫瘤學前沿科學中心(檔案編號:SP2021-00001-FSCPO、SP2023-00001-FSCPO)。全文可查閱:https://advanced.onlinelibrary.wiley.com/doi/full/10.1002/advs.202416811。
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https://www.um.edu.mo/zh-hant/news-and-press-releases/press-release/detail/60751/
UM research team proposes new approach to treating muscle atrophy
A research team led by Kathy Luo Qian, professor in the Faculty of Health Sciences (FHS) at the University of Macau (UM), has developed new models of muscle atrophy using sensor zebrafish. The study shows that atrophied muscles can improve overall muscle mass and strength by increasing the size of individual muscle cells, ultimately improving patients’ mobility and health. These findings offer new insights and ideas for the treatment of muscle atrophy. The research has been published in the internationally renowned journal Advanced Science.
Muscle atrophy can occur as a result of a number of conditions, including aging, prolonged bed rest, starvation, nerve injury, or diseases such as cancer, leading to reduced mobility. Over the past few decades, many methods have been used to treat muscle atrophy, including exercise, electrical stimulation, ultrasound therapy, and nutritional therapy. However, the results of these methods are not satisfactory. In muscle atrophy, the reduction in muscle mass can be attributed to either the death of muscle cells or the shrinkage of individual muscle fibres. Understanding this is therefore crucial to the treatment of diseases associated with muscle atrophy and to improving health outcomes.
To accurately detect muscle cell apoptosis, the research team developed a method for real-time tracking of muscle cell apoptosis in live zebrafish. They specifically expressed a genetically encoded fluorescent protein sensor in the muscle tissues of zebrafish. The sensor emits green fluorescence in live cells and blue fluorescence in apoptotic cells. Using these sensor zebrafish, the team found that in starvation-induced muscle atrophy, muscle cells shrank significantly but did not die. These atrophied muscle cells survived by engulfing their own cellular components, a process known as autophagy. When the zebrafish were refed, the autophagic vacuoles disappeared, indicating that muscle atrophy is reversible.
Zebrafish typically live for three to five years. To study aging-induced muscle atrophy, the research team followed zebrafish with fluorescent sensors for five years. They found that in aged zebrafish with muscle atrophy, muscle cells remained viable despite a 57% reduction in diameter. Gene expression analysis revealed a significant downregulation of apoptosis-related genes and an upregulation of autophagy-related genes.
The study found that in muscle atrophy caused by starvation and aging, muscle cells do not die but remain alive through autophagy. It also suggests that increasing the size of individual muscle cells can increase overall muscle mass and strength, ultimately improving patients’ mobility and health.
Prof Luo is the corresponding author of this study, and Jia Hao, a postdoctoral researcher in FHS, is the first author. PhD graduates Wu Renfei and Yang Hongmei also contributed to the research. The study received important support from the Animal Research Core and the Biological Imaging and Stem Cell Core of FHS. The research was funded by UM (File No.: MYRG2020-00121-FHS and MYRG2022-00025-FHS), the Science and Technology Development Fund of the Macao SAR (File No.: 0147/2020/A3, 044/2021/APD, and 0004/2021/AKP), and the Ministry of Education Frontiers Science Center for Precision Oncology, UM (File No.: SP2021-00001-FSCPO and SP2023-00001-FSCPO). The full text of the research article is available at https://advanced.onlinelibrary.wiley.com/doi/full/10.1002/advs.202416811.
To read the news on UM’s official website, please visit the following link:
https://www.um.edu.mo/news-and-press-releases/press-release/detail/60751/