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The Interplay between Autophagy and Redox Signaling in Cardiovascular Diseases
Barbora Boťanská1, Ima Dovinová1, Miroslav Barančík1
1Centre of Experimental Medicine, Institute for Heart Research, Slovak Academy of Sciences, Dúbravská Cesta 9, 84104 Bratislava, Slovakia.
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.
Insights
Oxidative stress from reactive species contributes to diseases. This review highlights how Nrf2 and autophagy pathways interact to regulate cellular redox balance and combat disease progression, particularly in cardiovascular conditions.
Area of Science:
- Cellular biology
- Molecular medicine
- Pathophysiology
Background:
- Reactive oxygen and nitrogen species (ROS/RNS) are signaling molecules at low levels but cause oxidative stress and disease at high levels.
- Oxidative stress is implicated in cardiovascular, metabolic, neurodegenerative diseases, diabetes, and cancer.
- Cellular defense systems maintaining redox homeostasis are crucial for responding to oxidative stress.
Purpose of the Study:
- To review the role of Nrf2 in redox regulation and cellular response to oxidative stress.
- To summarize current knowledge on autophagy regulation and the influence of redox signaling.
- To detail the interplay between Nrf2 and autophagy in myocardial cells and their role in cardiovascular disease.
Main Methods:
- Literature review focusing on Nrf2, autophagy, redox signaling, and oxidative stress.
- Analysis of the interface between Nrf2 and autophagy pathways.
- Examination of their specific roles in cardiovascular disease development.
Main Results:
- Nrf2 is a central regulator of cellular defense against oxidative stress.
- Autophagy is modulated by redox signaling pathways.
- A significant interplay exists between Nrf2 and autophagy in the context of oxidative stress and disease.
Conclusions:
- Nrf2 and autophagy are critical interconnected pathways in managing oxidative stress.
- Dysregulation of these pathways contributes to the progression of oxidative stress-induced diseases, especially cardiovascular diseases.
- Understanding the Nrf2-autophagy axis offers potential therapeutic targets for disease treatment.
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