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自噬与氧化应激信号在心血管疾病中的相互作用。

The Interplay between Autophagy and Redox Signaling in Cardiovascular Diseases.

机构信息

Centre of Experimental Medicine, Institute for Heart Research, Slovak Academy of Sciences, Dúbravská Cesta 9, 84104 Bratislava, Slovakia.

出版信息

Cells. 2022 Apr 2;11(7):1203. doi: 10.3390/cells11071203.

Abstract

Reactive oxygen and nitrogen species produced at low levels under normal cellular metabolism act as important signal molecules. However, at increased production, they cause damage associated with oxidative stress, which can lead to the development of many diseases, such as cardiovascular, metabolic, neurodegenerative, diabetes, and cancer. The defense systems used to maintain normal redox homeostasis plays an important role in cellular responses to oxidative stress. The key players here are Nrf2-regulated redox signaling and autophagy. A tight interface has been described between these two processes under stress conditions and their role in oxidative stress-induced diseases progression. In this review, we focus on the role of Nrf2 as a key player in redox regulation in cell response to oxidative stress. We also summarize the current knowledge about the autophagy regulation and the role of redox signaling in this process. In line with the focus of our review, we describe in more detail information about the interplay between Nrf2 and autophagy pathways in myocardium and the role of these processes in cardiovascular disease development.

摘要

在正常细胞代谢下低水平产生的活性氧和氮物种作为重要的信号分子发挥作用。然而,在产生增加时,它们会导致与氧化应激相关的损伤,从而导致许多疾病的发展,如心血管、代谢、神经退行性、糖尿病和癌症。用于维持正常氧化还原稳态的防御系统在细胞对氧化应激的反应中起着重要作用。这里的关键参与者是 Nrf2 调节的氧化还原信号和自噬。在应激条件下,已经描述了这两个过程之间的紧密接口及其在氧化应激诱导的疾病进展中的作用。在这篇综述中,我们重点介绍了 Nrf2 作为细胞对氧化应激反应中氧化还原调节的关键因子的作用。我们还总结了目前关于自噬调节和氧化还原信号在这一过程中的作用的知识。根据我们综述的重点,我们更详细地描述了 Nrf2 和自噬途径在心肌中的相互作用以及这些过程在心血管疾病发展中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8205/8997791/52eaa98882d8/cells-11-01203-g001.jpg

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