Mitochondria and the Pathophysiological Mechanism of Atrial Fibrillation

Title:Mitochondria and the Pathophysiological Mechanism of Atrial Fibrillation

Volume: 24 Issue: 26

Author(s): Xinye Li, Xinyu Yang, Yanda Li, Mengchen Yuan, Chao Tian, Yihan Yang, Xiaoyu Zhang, Chao Liu, Yonghong Gao, Nian Liu, Hongcai Shang*Yanwei Xing*

Affiliation:

• Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700,China

• Guang'an men Hospital, Chinese Academy of Chinese Medical Sciences, Beijing 100053,China

Keywords: Atrial fibrillation, mitochondria, pathophysiological mechanism, treatment, cardiac arrhythmia, reactive oxygen species.

Abstract: Atrial fibrillation (AF) is the most common and significant cardiac arrhythmia in clinical practice, however the pathophysiological mechanism of AF has not been fully explained. At present, there are no available treatment options that can target the underlying pathophysiological processes of AF. Research on improving management strategies for AF can start with a further understanding of the changes of cells in AF. Mitochondria play central roles in the function of cardiac myocytes and many of the pathophysiological processes implicated in AF are relative to mitochondrial function, including formation of reactive oxygen species (ROS), calcium homeostasis, and alterations of oxygen consumption. The changes of levels of phosphocreatine, electron transfer chain proteins and differences in mitochondrial distribution further imply that mitochondria play a role in AF. Related studies of recent years are summarized, in order to elucidate the causal relationship between mitochondria and AF, and provide potential therapeutic target for the treatment and prevention of AF in clinical practice. In the article, we summarize the direct or indirect factors that affect mitochondria function and thus cause AF, including anticancer agents, surgery, gene, age, air pollution, oxidative stress, and β3-adrenoceptor (β3-AR). There is a close relationship between mitochondrial dysfunction and the occurrence of AF, which cannot be ignored, and further research in this area is needed.

Cite this article as:

Li Xinye, Yang Xinyu , Li Yanda , Yuan Mengchen, Tian Chao , Yang Yihan , Zhang Xiaoyu , Liu Chao , Gao Yonghong , Liu Nian , Shang Hongcai *, Xing Yanwei *, Mitochondria and the Pathophysiological Mechanism of Atrial Fibrillation, Current Pharmaceutical Design 2018; 24 (26) . https://dx.doi.org/10.2174/1381612824666180903125300