标题：Metabolic Reprogramming of Human Cells in Response to Oxidative Stress: Implications in the Pathophysiology and Therapy of Mitochondrial Diseases

作者：Yu-Ting Wu Shi-Bei Wu Shi-Bei Wu Yau-Huei Wei Yau-Huei Wei

网址:

求助者：网友

• 求助时间：2015/6/30 18:08:36
• 求助状态：AB图书馆客服已找到全文，详情咨询在线客服qq 1257749646
• 文献摘要：

Mitochondria are the organelles producing most of the energy and play important roles in a variety of biochemical functions in human cells. Mitochondrial defects can cause ATP deficiency and overproduction of reactive oxygen species, which are the major hallmarks of mitochondrial diseases. Abundant evidence has suggested that mitochondrial dysfunction-elicited oxidative stress can play an important role in the pathogenesis and progression of mitochondrial diseases. Mitochondria can respond to energy deficiency by the retrograde signaling to trigger a number of molecular events to help the human cells to cope with physiological or environmental changes. In this article, we first describe oxidative stress-induced cellular responses including metabolic adaptation, compensatory increase of mitochondrial biogenesis, upregulation of antioxidant enzymes, and alteration of protein acetylation in human cells with mitochondrial dysfunction. In this regard, we review recent findings to elucidate the mechanisms by which human cells motivate their mitochondria and the antioxidant defense system to respond to energy deficiency and oxidative stress, which contribute to the adaptive metabolic reprogramming in mitochondrial diseases. In addition, we emphasize the critical role of the activation of AMPK and Sirt1 and Sirt3 in the metabolic adaptation of human cells harboring mitochondrial DNA mutations. Recent studies have revealed that AMPK and sirtuins-mediated signaling pathways are involved in metabolic reprogramming, which is effected by upregulation of antioxidant defense system and mitochondrial protein acetylation, in human cells with mitochondrial dysfunction. Finally, we discuss several potential modulators of bioenergetic function such as coenzyme Q10, mitochondria-targeting antioxidants, resveratrol, and L-carnitine based on recent findings from studies on human cells and animal models of mitochondrial diseases. Elucidation of the signaling pathway of this adaptive response to oxidative stress triggered by mitochondrial dysfunction may enable us to gain a deeper insight into the communication between mitochondria and the nucleus and guide us to develop novel therapeutic agents for effective treatment of mitochondrial diseases.

文献《Metabolic Reprogramming of Human Cells in Response to Oxidative Stress: Implications in the Pathophysiology and Therapy of Mitochondrial Diseases》已经找到全文，详情请咨询在线客服 qq 1257749646。
如果您还有其他需要寻找全文的文献，请点击文献求助提交

说明：文献求助是指AB图书馆根据读者的需求，为读者查找论文资料的服务。如果您搜索到相关资料，但不能获取全文，此时便可将有关信息提交求助，由值班客服为您寻找所需文献的全文。提供的文献均来自网络共享资源，不涉及版权交易；如侵犯了您的权利，请告知在线客服，立马删除。文件格式以PDF格式为主。