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线粒体疗法在治疗衰老过程中的氧化应激和炎症方面的潜力。

The Potential of Mitochondrial Therapeutics in the Treatment of Oxidative Stress and Inflammation in Aging.

作者信息

Sinha Jitendra Kumar, Jorwal Khanak, Singh Krishna Kumar, Han Sung Soo, Bhaskar Rakesh, Ghosh Shampa

机构信息

GloNeuro, Sector 107, Vishwakarma Road, Noida, Uttar Pradesh, 201301, India.

Symbiosis Centre for Information Technology, Symbiosis International (Deemed University), Pune, Maharashtra, 411057, India.

出版信息

Mol Neurobiol. 2025 Jun;62(6):6748-6763. doi: 10.1007/s12035-024-04474-0. Epub 2024 Sep 4.

Abstract

Mitochondria are central to cellular energy production, and their dysfunction is a major contributor to oxidative stress and chronic inflammation, pivotal factors in aging, and related diseases. With aging, mitochondrial efficiency declines, leading to an increase in ROS and persistent inflammatory responses. Therapeutic interventions targeting mitochondrial health show promise in mitigating these detrimental effects. Antioxidants such as MitoQ and MitoVitE, and supplements like coenzyme Q10 and NAD + precursors, have demonstrated potential in reducing oxidative stress. Additionally, gene therapy aimed at enhancing mitochondrial function, alongside lifestyle modifications such as regular exercise and caloric restriction can ameliorate age-related mitochondrial decline. Exercise not only boosts mitochondrial biogenesis but also improves mitophagy. Enhancing mitophagy is a key strategy to prevent the accumulation of dysfunctional mitochondria, which is crucial for cellular homeostasis and longevity. Pharmacological agents like sulforaphane, SS-31, and resveratrol indirectly promote mitochondrial biogenesis and improve cellular resistance to oxidative damage. The exploration of mitochondrial therapeutics, including emerging techniques like mitochondrial transplantation, offers significant avenues for extending health span and combating age-related diseases. However, translating these findings into clinical practice requires overcoming challenges in precisely targeting dysfunctional mitochondria and optimizing delivery mechanisms for therapeutic agents. Continued research is essential to refine these approaches and fully understand the interplay between mitochondrial dynamics and aging.

摘要

线粒体是细胞能量产生的核心,其功能障碍是氧化应激和慢性炎症的主要促成因素,而氧化应激和慢性炎症是衰老及相关疾病的关键因素。随着年龄增长,线粒体效率下降,导致活性氧增加和持续的炎症反应。针对线粒体健康的治疗干预措施在减轻这些有害影响方面显示出前景。抗氧化剂如MitoQ和MitoVitE,以及辅酶Q10和NAD+前体等补充剂,已证明在减少氧化应激方面具有潜力。此外,旨在增强线粒体功能的基因治疗,连同规律运动和热量限制等生活方式的改变,可以改善与年龄相关的线粒体衰退。运动不仅能促进线粒体生物发生,还能改善线粒体自噬。增强线粒体自噬是防止功能失调的线粒体积累的关键策略,这对细胞内稳态和长寿至关重要。萝卜硫素、SS-31和白藜芦醇等药物间接促进线粒体生物发生,并提高细胞对氧化损伤的抵抗力。对线粒体治疗方法的探索,包括线粒体移植等新兴技术,为延长健康寿命和对抗与年龄相关的疾病提供了重要途径。然而,将这些发现转化为临床实践需要克服精确靶向功能失调的线粒体以及优化治疗药物递送机制方面的挑战。持续的研究对于完善这些方法并充分理解线粒体动态与衰老之间的相互作用至关重要。

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