中文摘要：

與肌肉減少癥相關(guān)的肌肉無力是導(dǎo)致老年人健康壽命和生活質(zhì)量下降的主要原因。然而，衰老中肌肉無力的潛在機(jī)制尚未明確。我們研究了氧化應(yīng)激和衰老對缺乏抗氧化酶 CuZnSod （Sod1KO） 的小鼠和衰老 （24 個月大） 野生型小鼠和皮膚透化單纖維產(chǎn)生肌肉力的特定分子機(jī)制的影響。兩種模型都發(fā)生肌肉力量損失，可能是因為膜興奮性降低，NKA 信號傳導(dǎo)和 RyR 穩(wěn)定性改變，纖維 Ca2+ 敏感性降低，并通過修飾 Cys674 殘基抑制 SERCA 活性，SR 失調(diào)和胞質(zhì) Ca2+ 穩(wěn)態(tài)，以及線粒體 Ca2+ 緩沖和呼吸受損。我們的結(jié)果提供了對衰老和氧化應(yīng)激對肌肉無力相關(guān)機(jī)制的具體影響的更好理解，這可能為未來對抗肌肉無力的干預(yù)措施指明方向。

英文摘要：

Muscle weakness associated with sarcopenia is a major contributor to reduced health span and quality of life in the elderly. However, the underlying mechanisms of muscle weakness in aging are not fully defined. We investigated the effect of oxidative stress and aging on specific molecular mechanisms involved in muscle force production in mice and skinned permeabilized single fibers in mice lacking the antioxidant enzyme CuZnSod (Sod1KO) and in aging (24-month-old) wild-type mice. Loss of muscle strength occurs in both models, potentially because of reduced membrane excitability with altered NKA signaling and RyR stability, decreased fiber Ca2+ sensitivity and suppressed SERCA activity via modification of the Cys674 residue, dysregulated SR and cytosolic Ca2+ homeostasis, and impaired mitochondrial Ca2+ buffering and respiration. Our results provide a better understanding of the specific impacts of aging and oxidative stress on mechanisms related to muscle weakness that may point to future interventions for countering muscle weakness.

論文信息：

論文題目：Impact of aging and oxidative stress on specific components of excitation contraction coupling in regulating force generation

期刊名稱：SCIENCE ADVANCES

時間期卷： Vol 8, Issue 43

在線時間：2022年10月26日

DOI： 10.1126/sciadv.add7377

Virogen抗谷胱甘肽抗體貨號101-A檢測圖：

Virogen抗體101-A引用截圖：

Virogen抗谷胱甘肽Anti-Glutathione antibody抗體 抗谷胱甘肽小鼠單克隆抗體 Anti-Glutathione monoclonal antibody 產(chǎn)品編號:101-A。該抗體檢測谷胱甘肽 谷胱甘肽是啥: 谷胱甘肽是一種普遍存在于動物、植物和部分細(xì)菌體內(nèi)的抗氧化劑,能夠清除活性氧自由基,阻止脂質(zhì)過氧化。