Bhutada Sahil P, Agrawal Ishwar, Punpale Ajinklya, Kannure Viresh, Prasad Roshan, Lohakare Tejaswee, Wanjari Mayur, Mittal Gaurav
Medicine, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education and Research, Wardha, IND.
Surgical Oncology, Jawaharlal Nehru Medical College, Datta Meghe Institute of Higher Education and Research, Wardha, IND.
Cureus. 2023 Aug 30;15(8):e44367. doi: 10.7759/cureus.44367. eCollection 2023 Aug.
Oxidative stress has emerged as a significant contributor to skeletal muscle atrophy, influencing cellular processes that underlie muscle wasting. This review article delves into the intricate interplay between oxidative stress and muscle atrophy, shedding light on its mechanisms and implications. We begin by outlining the fundamental concepts of oxidative stress, delineating reactive oxygen species (ROS) and reactive nitrogen species (RNS), their sources, and the ensuing oxidative damage to cellular components. Subsequently, we delve into skeletal muscle atrophy, elucidating its diverse forms, molecular pathways, key signaling cascades, and the role of inflammation in exacerbating muscle wasting. Bridging these concepts, we explore the connections between oxidative stress and muscle atrophy, unveiling how oxidative stress impacts muscle protein synthesis and breakdown, perturbs cellular signaling pathways, and contributes to mitochondrial dysfunction. The review underscores the complexity of quantifying and interpreting oxidative stress markers, highlighting the challenges posed by the dynamic nature of oxidative stress and the presence of basal ROS levels. Addressing the specificity of oxidative stress markers, we emphasize the importance of selecting markers pertinent to muscle tissue and considering systemic influences. Standardization of experimental protocols emerges as a critical need to ensure consistency and reproducibility across studies. Looking ahead, we discuss the implications of oxidative stress in diverse scenarios, encompassing age-related muscle loss (sarcopenia), muscle wasting in chronic diseases like cancer cachexia, and disuse-induced muscle atrophy. Additionally, we delve into potential therapeutic strategies, including antioxidant supplementation, exercise, pharmacological interventions, nutritional approaches, and lifestyle modifications, as avenues to mitigate oxidative stress-driven muscle atrophy. The review concludes by outlining promising future directions in this field, calling for deeper exploration of specific oxidative stress markers, understanding the temporal dynamics of oxidative stress, validation through translational studies in humans, and the development of targeted therapeutic interventions. By advancing our understanding of the intricate relationship between oxidative stress and skeletal muscle atrophy, this review contributes to paving the way for innovative strategies to address muscle wasting and improve muscle health.
氧化应激已成为骨骼肌萎缩的一个重要促成因素，影响着导致肌肉消瘦的细胞过程。这篇综述文章深入探讨了氧化应激与肌肉萎缩之间的复杂相互作用，阐明了其机制和影响。我们首先概述氧化应激的基本概念，描述活性氧（ROS）和活性氮（RNS）、它们的来源以及随后对细胞成分的氧化损伤。随后，我们深入研究骨骼肌萎缩，阐明其多种形式、分子途径、关键信号级联以及炎症在加剧肌肉消瘦中的作用。将这些概念联系起来，我们探索氧化应激与肌肉萎缩之间的联系，揭示氧化应激如何影响肌肉蛋白质合成和分解、扰乱细胞信号通路并导致线粒体功能障碍。该综述强调了量化和解释氧化应激标志物的复杂性，突出了氧化应激的动态性质和基础ROS水平的存在所带来的挑战。在讨论氧化应激标志物的特异性时，我们强调选择与肌肉组织相关的标志物并考虑全身影响的重要性。实验方案的标准化成为确保各研究之间一致性和可重复性的迫切需求。展望未来，我们讨论氧化应激在各种情况下的影响，包括与年龄相关的肌肉减少（肌肉减少症）、癌症恶病质等慢性疾病中的肌肉消瘦以及废用性肌肉萎缩。此外，我们深入探讨潜在的治疗策略，包括抗氧化剂补充、运动、药物干预、营养方法和生活方式改变，作为减轻氧化应激驱动的肌肉萎缩的途径。综述最后概述了该领域有前景的未来方向，呼吁更深入地探索特定的氧化应激标志物、了解氧化应激的时间动态、通过人体转化研究进行验证以及开发有针对性的治疗干预措施。通过增进我们对氧化应激与骨骼肌萎缩之间复杂关系的理解，这篇综述有助于为解决肌肉消瘦和改善肌肉健康的创新策略铺平道路。
