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,...
Saved in:
Main Authors: | , , , |
---|---|
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 |