Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation

Mitophagy is an autophagic response and plays essential roles in survival, development, and homeostasis of cells. It has been reported that mitophagic dysfunction is involved in several cardiovascular diseases. However, the effect of mitophagy on atrial fibrillation (AF) is still unknown. Therefore,...

Full description

Saved in:
Bibliographic Details
Main Authors: Shuang Zhou, Weiran Dai, Guoqiang Zhong, Zhiyuan Jiang
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Cardiology Research and Practice
Online Access:http://dx.doi.org/10.1155/2020/6757350
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832560324585193472
author Shuang Zhou
Weiran Dai
Guoqiang Zhong
Zhiyuan Jiang
author_facet Shuang Zhou
Weiran Dai
Guoqiang Zhong
Zhiyuan Jiang
author_sort Shuang Zhou
collection DOAJ
description Mitophagy is an autophagic response and plays essential roles in survival, development, and homeostasis of cells. It has been reported that mitophagic dysfunction is involved in several cardiovascular diseases. However, the effect of mitophagy on atrial fibrillation (AF) is still unknown. Therefore, we investigated the exact role of mitophagy in human chronic AF. Western blot was used to detect the protein abundance. The mitochondrial morphology and structure were observed by transmission electron microscopy. Immunofluorescent stainings were performed to analyze colocalization of mitochondria with autophagosomes or lysosomes. Totally, 43 patients with valvular heart disease undergoing cardiac surgery were selected, including 21 patients with chronic AF. Comparing with the sinus rhythm (SR) group, we found the size and number of mitochondria in atrial myocytes of patients with AF increased significantly. In addition, expression of LC3B II and LC3B II/LC3B I ratio was significantly decreased in the AF group. Moreover, the expression of p62 was markedly elevated in the AF group compared with that in the SR group. The results of immunofluorescence staining and western blot showed an enhanced expression of Cox IV in the AF group. Dual immunofluorescent stainings revealed that mitophagy defect in atrial myocytes of patients with AF resulted from dysfunction in the process of delivery of mitochondria into autophagosomes. For the first time, impaired mitophagy, during the phagocytosis of mitochondria, is associated with human chronic AF. Mitophagy could be a potential therapeutic target for AF.
format Article
id doaj-art-857db5217665402a91329395ce554807
institution Kabale University
issn 2090-8016
2090-0597
language English
publishDate 2020-01-01
publisher Wiley
record_format Article
series Cardiology Research and Practice
spelling doaj-art-857db5217665402a91329395ce5548072025-02-03T01:27:57ZengWileyCardiology Research and Practice2090-80162090-05972020-01-01202010.1155/2020/67573506757350Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial FibrillationShuang Zhou0Weiran Dai1Guoqiang Zhong2Zhiyuan Jiang3Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Cardiovascular Institute, Nanning, Guangxi, ChinaDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Cardiovascular Institute, Nanning, Guangxi, ChinaDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Cardiovascular Institute, Nanning, Guangxi, ChinaDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, Guangxi Cardiovascular Institute, Nanning, Guangxi, ChinaMitophagy is an autophagic response and plays essential roles in survival, development, and homeostasis of cells. It has been reported that mitophagic dysfunction is involved in several cardiovascular diseases. However, the effect of mitophagy on atrial fibrillation (AF) is still unknown. Therefore, we investigated the exact role of mitophagy in human chronic AF. Western blot was used to detect the protein abundance. The mitochondrial morphology and structure were observed by transmission electron microscopy. Immunofluorescent stainings were performed to analyze colocalization of mitochondria with autophagosomes or lysosomes. Totally, 43 patients with valvular heart disease undergoing cardiac surgery were selected, including 21 patients with chronic AF. Comparing with the sinus rhythm (SR) group, we found the size and number of mitochondria in atrial myocytes of patients with AF increased significantly. In addition, expression of LC3B II and LC3B II/LC3B I ratio was significantly decreased in the AF group. Moreover, the expression of p62 was markedly elevated in the AF group compared with that in the SR group. The results of immunofluorescence staining and western blot showed an enhanced expression of Cox IV in the AF group. Dual immunofluorescent stainings revealed that mitophagy defect in atrial myocytes of patients with AF resulted from dysfunction in the process of delivery of mitochondria into autophagosomes. For the first time, impaired mitophagy, during the phagocytosis of mitochondria, is associated with human chronic AF. Mitophagy could be a potential therapeutic target for AF.http://dx.doi.org/10.1155/2020/6757350
spellingShingle Shuang Zhou
Weiran Dai
Guoqiang Zhong
Zhiyuan Jiang
Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation
Cardiology Research and Practice
title Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation
title_full Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation
title_fullStr Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation
title_full_unstemmed Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation
title_short Impaired Mitophagy: A New Potential Mechanism of Human Chronic Atrial Fibrillation
title_sort impaired mitophagy a new potential mechanism of human chronic atrial fibrillation
url http://dx.doi.org/10.1155/2020/6757350
work_keys_str_mv AT shuangzhou impairedmitophagyanewpotentialmechanismofhumanchronicatrialfibrillation
AT weirandai impairedmitophagyanewpotentialmechanismofhumanchronicatrialfibrillation
AT guoqiangzhong impairedmitophagyanewpotentialmechanismofhumanchronicatrialfibrillation
AT zhiyuanjiang impairedmitophagyanewpotentialmechanismofhumanchronicatrialfibrillation