Mitophagy deficiency activates stimulator of interferon genes activation and aggravates pathogenetic cardiac remodeling

Stimulator of interferon genes (STING) has recently been found to play a crucial role in cardiac sterile inflammation and dysfunction. The role of stimulator of interferon genes (STING) in cardiac sterile inflammation and dysfunction has been recently discovered. This study aims to examine the invol...

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Published in:	Genes & diseases Vol. 11; no. 6; p. 101074
Main Authors:	Zhou, Guoxiang, Wang, Xiaowen, Guo, Mingyu, Qu, Can, Gao, Lei, Yu, Jiang, Li, Yuanjing, Luo, Suxin, Shi, Qiong, Guo, Yongzheng
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier B.V 01.11.2024 KeAi Communications Co., Ltd
Subjects:	Cardiac remodeling Mitochondrial autophagy mtDNA Sterile inflammation STING STING Cardiac remodeling Sterile inflammation Mitochondrial autophagy mtDNA
ISSN:	2352-3042, 2352-3042
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Abstract	Stimulator of interferon genes (STING) has recently been found to play a crucial role in cardiac sterile inflammation and dysfunction. The role of stimulator of interferon genes (STING) in cardiac sterile inflammation and dysfunction has been recently discovered. This study aims to examine the involvement of STING in pathological cardiac remodeling and the mechanisms that govern the activation of the STING pathway. To investigate this, transverse aortic constriction (TAC) was performed on STING knockout mice to induce pressure overload-induced cardiac remodeling. Subsequently, cardiac function, remodeling, and inflammation levels were evaluated. The STING pathway was found to be activated in the pressure overload-stressed heart and angiotensin II (Ang II)-stimulated cardiac fibroblasts. Loss of STING expression led to a significant reduction in inflammatory responses, mitochondrial fragmentation, and oxidative stress in the heart, resulting in attenuated cardiac remodeling and dysfunction. Furthermore, the exacerbation of pressure overload-induced STING-mediated inflammation and pathological cardiac remodeling was observed when mitophagy was suppressed through the silencing of Parkin, an E3 ubiquitin ligase. Taken together, these findings indicate that STING represents a newly identified and significant molecule implicated in the process of pathological cardiac remodeling and that mitophagy is an upstream mechanism that regulates STING activation. Targeting STING may therefore provide a novel therapeutic strategy for pathological cardiac remodeling and heart failure.
AbstractList	Stimulator of interferon genes (STING) has recently been found to play a crucial role in cardiac sterile inflammation and dysfunction. The role of stimulator of interferon genes (STING) in cardiac sterile inflammation and dysfunction has been recently discovered. This study aims to examine the involvement of STING in pathological cardiac remodeling and the mechanisms that govern the activation of the STING pathway. To investigate this, transverse aortic constriction (TAC) was performed on STING knockout mice to induce pressure overload-induced cardiac remodeling. Subsequently, cardiac function, remodeling, and inflammation levels were evaluated. The STING pathway was found to be activated in the pressure overload-stressed heart and angiotensin II (Ang II)-stimulated cardiac fibroblasts. Loss of STING expression led to a significant reduction in inflammatory responses, mitochondrial fragmentation, and oxidative stress in the heart, resulting in attenuated cardiac remodeling and dysfunction. Furthermore, the exacerbation of pressure overload-induced STING-mediated inflammation and pathological cardiac remodeling was observed when mitophagy was suppressed through the silencing of Parkin, an E3 ubiquitin ligase. Taken together, these findings indicate that STING represents a newly identified and significant molecule implicated in the process of pathological cardiac remodeling and that mitophagy is an upstream mechanism that regulates STING activation. Targeting STING may therefore provide a novel therapeutic strategy for pathological cardiac remodeling and heart failure. Stimulator of interferon genes (STING) has recently been found to play a crucial role in cardiac sterile inflammation and dysfunction. The role of stimulator of interferon genes (STING) in cardiac sterile inflammation and dysfunction has been recently discovered. This study aims to examine the involvement of STING in pathological cardiac remodeling and the mechanisms that govern the activation of the STING pathway. To investigate this, transverse aortic constriction (TAC) was performed on STING knockout mice to induce pressure overload-induced cardiac remodeling. Subsequently, cardiac function, remodeling, and inflammation levels were evaluated. The STING pathway was found to be activated in the pressure overload-stressed heart and angiotensin II (Ang II)-stimulated cardiac fibroblasts. Loss of STING expression led to a significant reduction in inflammatory responses, mitochondrial fragmentation, and oxidative stress in the heart, resulting in attenuated cardiac remodeling and dysfunction. Furthermore, the exacerbation of pressure overload-induced STING-mediated inflammation and pathological cardiac remodeling was observed when mitophagy was suppressed through the silencing of Parkin, an E3 ubiquitin ligase. Taken together, these findings indicate that STING represents a newly identified and significant molecule implicated in the process of pathological cardiac remodeling and that mitophagy is an upstream mechanism that regulates STING activation. Targeting STING may therefore provide a novel therapeutic strategy for pathological cardiac remodeling and heart failure.Stimulator of interferon genes (STING) has recently been found to play a crucial role in cardiac sterile inflammation and dysfunction. The role of stimulator of interferon genes (STING) in cardiac sterile inflammation and dysfunction has been recently discovered. This study aims to examine the involvement of STING in pathological cardiac remodeling and the mechanisms that govern the activation of the STING pathway. To investigate this, transverse aortic constriction (TAC) was performed on STING knockout mice to induce pressure overload-induced cardiac remodeling. Subsequently, cardiac function, remodeling, and inflammation levels were evaluated. The STING pathway was found to be activated in the pressure overload-stressed heart and angiotensin II (Ang II)-stimulated cardiac fibroblasts. Loss of STING expression led to a significant reduction in inflammatory responses, mitochondrial fragmentation, and oxidative stress in the heart, resulting in attenuated cardiac remodeling and dysfunction. Furthermore, the exacerbation of pressure overload-induced STING-mediated inflammation and pathological cardiac remodeling was observed when mitophagy was suppressed through the silencing of Parkin, an E3 ubiquitin ligase. Taken together, these findings indicate that STING represents a newly identified and significant molecule implicated in the process of pathological cardiac remodeling and that mitophagy is an upstream mechanism that regulates STING activation. Targeting STING may therefore provide a novel therapeutic strategy for pathological cardiac remodeling and heart failure.
ArticleNumber	101074
Author	Gao, Lei Guo, Yongzheng Guo, Mingyu Qu, Can Shi, Qiong Wang, Xiaowen Li, Yuanjing Luo, Suxin Yu, Jiang Zhou, Guoxiang
Author_xml	– sequence: 1 givenname: Guoxiang surname: Zhou fullname: Zhou, Guoxiang organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 2 givenname: Xiaowen surname: Wang fullname: Wang, Xiaowen organization: Department of Cardiothoracic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 3 givenname: Mingyu surname: Guo fullname: Guo, Mingyu organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 4 givenname: Can surname: Qu fullname: Qu, Can organization: Department of Pharmacy, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 5 givenname: Lei surname: Gao fullname: Gao, Lei organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 6 givenname: Jiang surname: Yu fullname: Yu, Jiang organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 7 givenname: Yuanjing surname: Li fullname: Li, Yuanjing organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 8 givenname: Suxin surname: Luo fullname: Luo, Suxin organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China – sequence: 9 givenname: Qiong surname: Shi fullname: Shi, Qiong email: shiqiong@cqmu.edu.cn organization: The Department of Laboratory Medicine, M.O.E. Key Laboratory of Laboratory Medical Diagnostics, Chongqing Medical University, Chongqing 400016, China – sequence: 10 givenname: Yongzheng surname: Guo fullname: Guo, Yongzheng email: gyz_cardio@hospital.cqmu.edu.cn organization: Division of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
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Keywords	STING Cardiac remodeling Sterile inflammation Mitochondrial autophagy mtDNA
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Snippet	Stimulator of interferon genes (STING) has recently been found to play a crucial role in cardiac sterile inflammation and dysfunction. The role of stimulator...
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SubjectTerms	Cardiac remodeling Mitochondrial autophagy mtDNA Sterile inflammation STING
Title	Mitophagy deficiency activates stimulator of interferon genes activation and aggravates pathogenetic cardiac remodeling
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