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钠钾 ATP 酶信号在与衰老相关的氧化应激中的作用:肥胖和心血管疾病中的意义。

The Role of Na/K-ATPase Signaling in Oxidative Stress Related to Aging: Implications in Obesity and Cardiovascular Disease.

机构信息

Department of Internal Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25701, USA.

Department of Surgery and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA.

出版信息

Int J Mol Sci. 2018 Jul 23;19(7):2139. doi: 10.3390/ijms19072139.

DOI:10.3390/ijms19072139
PMID:30041449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6073138/
Abstract

Aging has been associated with a series of pathophysiological processes causing general decline in the overall health of the afflicted population. The cumulative line of evidence suggests an important role of oxidative stress in the development and progression of the aging process and metabolic abnormalities, exacerbating adipocyte dysfunction, cardiovascular diseases, and associated complications at the same time. In recent years, robust have established the implication of Na/K-ATPase signaling in causing oxidative stress and alterations in cellular mechanisms, in addition to its distinct pumping function. Understanding the underlying molecular mechanisms and exploring the possible sources of pro-oxidants may allow for developing therapeutic targets in these processes and formulate novel intervention strategies for patients susceptible to aging and associated complications, such as obesity and cardiovascular disease. The attenuation of oxidative stress with targeted treatment options can improve patient outcomes and significantly reduce economic burden.

摘要

衰老是与一系列病理生理过程相关联的,这些过程导致受影响人群的整体健康状况普遍下降。累积的证据表明,氧化应激在衰老过程和代谢异常的发展和进展中起着重要作用,同时加剧脂肪细胞功能障碍、心血管疾病和相关并发症。近年来,研究人员已经证实 Na/K-ATPase 信号在引起氧化应激和细胞机制改变方面的作用,除了其独特的泵送功能之外。了解潜在的分子机制并探索促氧化剂的可能来源,可能有助于针对这些过程开发治疗靶点,并为易患衰老和相关并发症(如肥胖和心血管疾病)的患者制定新的干预策略。通过有针对性的治疗选择来减轻氧化应激,可以改善患者的预后并显著减轻经济负担。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/0b9619cedc70/ijms-19-02139-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/c12f79c8f434/ijms-19-02139-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/73777203867f/ijms-19-02139-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/0b9619cedc70/ijms-19-02139-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/c12f79c8f434/ijms-19-02139-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/73777203867f/ijms-19-02139-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d744/6073138/0b9619cedc70/ijms-19-02139-g003.jpg

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