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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| Vydáno v: | Genes & diseases Ročník 11; číslo 6; s. 101074 |
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| Hlavní autoři: | , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Netherlands
Elsevier B.V
01.11.2024
KeAi Communications Co., Ltd |
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| 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. |
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| 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 |
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| Cites_doi | 10.1002/ejhf.942 10.1161/ATVBAHA.117.309017 10.3390/molecules24081583 10.1093/cvr/cvu264 10.1161/CIRCULATIONAHA.119.041460 10.1016/j.biopha.2020.110022 10.1161/CIRCRESAHA.117.310624 10.1007/s00395-019-0722-5 10.1016/j.yjmcc.2013.11.015 10.1038/s41586-018-0448-9 10.1016/j.redox.2019.101254 10.1093/cvr/cvy052 10.1073/pnas.1106291108 10.1038/nrcardio.2017.139 10.1016/j.cell.2014.11.036 10.1186/s12964-021-00793-0 10.1016/j.cmet.2019.08.003 10.1038/nature10992 10.1016/j.cub.2018.01.004 10.1161/CIRCRESAHA.117.312317 10.1126/science.1232458 10.1042/BCJ20170714 10.1161/CIRCULATIONAHA.114.011079 10.2174/1871529X11313020010 10.1002/iub.2339 10.1093/cvr/cvu062 10.1038/ni.3558 10.15252/embr.201949799 10.1073/pnas.1708744114 10.1016/j.mito.2017.10.009 10.1007/s00109-015-1254-6 10.1186/s10020-022-00554-w 10.1161/CIRCULATIONAHA.110.982777 10.1126/science.aad0116 10.1152/ajprenal.00554.2020 10.1161/CIRCULATIONAHA.117.031046 10.1113/JP271301 10.1038/nm.4428 10.1161/CIRCRESAHA.115.306565 10.3389/fimmu.2018.00536 10.3892/ijmm.2014.1650 10.1152/ajpheart.00097.2020 |
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| Keywords | STING Cardiac remodeling Sterile inflammation Mitochondrial autophagy mtDNA |
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| References | Piccoli, Gupta, Viereck (bib29) 2017; 121 Purnomo, Piccart, Coenen, Prihadi, Lijnen (bib38) 2013; 13 Billia, Hauck, Konecny, Rao, Shen, Mak (bib26) 2011; 108 King, Aguirre, Ye (bib6) 2017; 23 Luo, Wang, Zhang (bib33) 2020; 141 Guo, Wang, Qin (bib17) 2018; 114 van Linthout, Miteva, Tschöpe (bib31) 2014; 102 Harris, Deen, Zamani, Hasnat (bib44) 2018; 41 Kim, Uriel, Burkhoff (bib1) 2018; 15 Travers, Kamal, Robbins, Yutzey, Blaxall (bib2) 2016; 118 Gong, Lu, Zhou (bib24) 2021; 320 Shires, Gustafsson (bib19) 2015; 93 Zhuang, Ma, Xu, Sun (bib23) 2022; 28 Singh, Kukreti, Saso, Kukreti (bib40) 2019; 24 Sun, Wu, Du, Chen, Chen (bib10) 2013; 339 Chen, Sun, Chen (bib9) 2016; 17 Zhang, Chen, Wang (bib36) 2020; 125 Nakayama, Otsu (bib11) 2018; 475 Zhao, Viswanadhapalli, Williams (bib39) 2015; 131 Zhang, Bauersachs, Langer (bib4) 2017; 19 Mao, Luo, Zhang (bib34) 2017; 37 Wai, García-Prieto, Baker (bib18) 2015; 350 White, McArthur, Metcalf (bib27) 2014; 159 Wang, Nie, Wu (bib21) 2018; 122 Lin, Li, Jiang (bib22) 2019; 26 Shinde, Frangogiannis (bib25) 2014; 70 Kawaguchi, Takahashi, Hata (bib32) 2011; 123 Hu, Cui, Wu (bib35) 2020; 318 Cheng, Qi, Zhang, Mao (bib30) 2021; 5 Meyer, Laverny, Bernardi (bib12) 2018; 9 Hajouli, Ludhwani (bib5) December 23, 2022 Sliter, Martinez, Hao (bib45) 2018; 561 Xiong, Li, Chen (bib37) 2021; 19 Bacmeister, Schwarzl, Warnke (bib3) 2019; 114 Cartledge, Kane, Dias (bib28) 2015; 105 Zhang, Liu, Liu, Ren, Sun (bib42) 2014; 33 Riley, Tait (bib14) 2020; 21 Vásquez-Trincado, García-Carvajal, Pennanen (bib20) 2016; 594 Peng, Zhou, Guo, Cheng, Luo, Guo (bib7) 2023; 8 Cao, Schiattarella, Villalobos (bib8) 2018; 137 Nie, Lu, Wang, Gao (bib13) 2020; 72 Oka, Hikoso, Yamaguchi (bib15) 2012; 485 Bai, Cervantes, Liu (bib16) 2017; 114 Chung, Dhillon, Huang (bib41) 2019; 30 Pickles, Vigié, Youle (bib43) 2018; 28 Travers (10.1016/j.gendis.2023.08.003_bib2) 2016; 118 Singh (10.1016/j.gendis.2023.08.003_bib40) 2019; 24 Kim (10.1016/j.gendis.2023.08.003_bib1) 2018; 15 Billia (10.1016/j.gendis.2023.08.003_bib26) 2011; 108 Purnomo (10.1016/j.gendis.2023.08.003_bib38) 2013; 13 Shires (10.1016/j.gendis.2023.08.003_bib19) 2015; 93 Mao (10.1016/j.gendis.2023.08.003_bib34) 2017; 37 Vásquez-Trincado (10.1016/j.gendis.2023.08.003_bib20) 2016; 594 Zhao (10.1016/j.gendis.2023.08.003_bib39) 2015; 131 Lin (10.1016/j.gendis.2023.08.003_bib22) 2019; 26 Shinde (10.1016/j.gendis.2023.08.003_bib25) 2014; 70 Peng (10.1016/j.gendis.2023.08.003_bib7) 2023; 8 Luo (10.1016/j.gendis.2023.08.003_bib33) 2020; 141 King (10.1016/j.gendis.2023.08.003_bib6) 2017; 23 Zhang (10.1016/j.gendis.2023.08.003_bib42) 2014; 33 Sliter (10.1016/j.gendis.2023.08.003_bib45) 2018; 561 Zhuang (10.1016/j.gendis.2023.08.003_bib23) 2022; 28 Wang (10.1016/j.gendis.2023.08.003_bib21) 2018; 122 Pickles (10.1016/j.gendis.2023.08.003_bib43) 2018; 28 Bai (10.1016/j.gendis.2023.08.003_bib16) 2017; 114 Bacmeister (10.1016/j.gendis.2023.08.003_bib3) 2019; 114 Zhang (10.1016/j.gendis.2023.08.003_bib4) 2017; 19 Piccoli (10.1016/j.gendis.2023.08.003_bib29) 2017; 121 Cheng (10.1016/j.gendis.2023.08.003_bib30) 2021; 5 Zhang (10.1016/j.gendis.2023.08.003_bib36) 2020; 125 Xiong (10.1016/j.gendis.2023.08.003_bib37) 2021; 19 Hu (10.1016/j.gendis.2023.08.003_bib35) 2020; 318 Chen (10.1016/j.gendis.2023.08.003_bib9) 2016; 17 Sun (10.1016/j.gendis.2023.08.003_bib10) 2013; 339 Gong (10.1016/j.gendis.2023.08.003_bib24) 2021; 320 Cao (10.1016/j.gendis.2023.08.003_bib8) 2018; 137 Oka (10.1016/j.gendis.2023.08.003_bib15) 2012; 485 Hajouli (10.1016/j.gendis.2023.08.003_bib5) 2022 Meyer (10.1016/j.gendis.2023.08.003_bib12) 2018; 9 Chung (10.1016/j.gendis.2023.08.003_bib41) 2019; 30 Nie (10.1016/j.gendis.2023.08.003_bib13) 2020; 72 Wai (10.1016/j.gendis.2023.08.003_bib18) 2015; 350 Nakayama (10.1016/j.gendis.2023.08.003_bib11) 2018; 475 Riley (10.1016/j.gendis.2023.08.003_bib14) 2020; 21 Harris (10.1016/j.gendis.2023.08.003_bib44) 2018; 41 White (10.1016/j.gendis.2023.08.003_bib27) 2014; 159 Kawaguchi (10.1016/j.gendis.2023.08.003_bib32) 2011; 123 Guo (10.1016/j.gendis.2023.08.003_bib17) 2018; 114 van Linthout (10.1016/j.gendis.2023.08.003_bib31) 2014; 102 Cartledge (10.1016/j.gendis.2023.08.003_bib28) 2015; 105 |
| References_xml | – volume: 23 start-page: 1481 year: 2017 end-page: 1487 ident: bib6 article-title: IRF publication-title: Nat Med – volume: 9 start-page: 536 year: 2018 ident: bib12 article-title: Mitochondria: an organelle of bacterial origin controlling inflammation publication-title: Front Immunol – volume: 122 start-page: 712 year: 2018 end-page: 729 ident: bib21 article-title: AMPKα2 protects against the development of heart failure by enhancing mitophagy via PINK1 phosphorylation publication-title: Circ Res – volume: 320 start-page: F608 year: 2021 end-page: F616 ident: bib24 article-title: The novel STING antagonist H151 ameliorates cisplatin-induced acute kidney injury and mitochondrial dysfunction publication-title: Am J Physiol Ren Physiol – volume: 15 start-page: 83 year: 2018 end-page: 96 ident: bib1 article-title: Reverse remodelling and myocardial recovery in heart failure publication-title: Nat Rev Cardiol – volume: 8 year: 2023 ident: bib7 article-title: Inhibition of publication-title: Cardiovasc Innov Appl – volume: 72 start-page: 1879 year: 2020 end-page: 1890 ident: bib13 article-title: Pro-inflammatory role of cell-free mitochondrial DNA in cardiovascular diseases publication-title: IUBMB Life – volume: 159 start-page: 1549 year: 2014 end-page: 1562 ident: bib27 article-title: Apoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production publication-title: Cell – volume: 131 start-page: 643 year: 2015 end-page: 655 ident: bib39 article-title: NADPH oxidase 4 induces cardiac fibrosis and hypertrophy through activating Akt/mTOR and NFκB signaling pathways publication-title: Circulation – volume: 141 start-page: 42 year: 2020 end-page: 66 ident: bib33 article-title: Critical role of cytosolic DNA and its sensing adaptor STING in aortic degeneration, dissection, and rupture publication-title: Circulation – volume: 118 start-page: 1021 year: 2016 end-page: 1040 ident: bib2 article-title: Cardiac fibrosis: the fibroblast awakens publication-title: Circ Res – volume: 41 start-page: 2 year: 2018 end-page: 8 ident: bib44 article-title: Mitophagy and the release of inflammatory cytokines publication-title: Mitochondrion – volume: 17 start-page: 1142 year: 2016 end-page: 1149 ident: bib9 article-title: Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing publication-title: Nat Immunol – volume: 318 start-page: H1525 year: 2020 end-page: H1537 ident: bib35 article-title: Cytosolic DNA sensor cGAS plays an essential pathogenetic role in pressure overload-induced heart failure publication-title: Am J Physiol Heart Circ Physiol – volume: 70 start-page: 74 year: 2014 end-page: 82 ident: bib25 article-title: Fibroblasts in myocardial infarction: a role in inflammation and repair publication-title: J Mol Cell Cardiol – volume: 125 year: 2020 ident: bib36 article-title: STING is an essential regulator of heart inflammation and fibrosis in mice with pathological cardiac hypertrophy via endoplasmic reticulum (ER) stress publication-title: Biomed Pharmacother – volume: 33 start-page: 817 year: 2014 end-page: 824 ident: bib42 article-title: Mitochondrial DNA induces inflammation and increases TLR9/NF-κB expression in lung tissue publication-title: Int J Mol Med – volume: 30 start-page: 784 year: 2019 end-page: 799.e5 ident: bib41 article-title: Mitochondrial damage and activation of the STING pathway lead to renal inflammation and fibrosis publication-title: Cell Metabol – volume: 19 start-page: 1379 year: 2017 end-page: 1389 ident: bib4 article-title: Immune mechanisms in heart failure publication-title: Eur J Heart Fail – volume: 5 start-page: 267 year: 2021 end-page: 274 ident: bib30 article-title: Myocardial fibrosis in the pathogenesis, diagnosis, and treatment of hypertrophic cardiomyopathy publication-title: Cardiovasc Innov Appl – volume: 114 start-page: 19 year: 2019 ident: bib3 article-title: Inflammation and fibrosis in murine models of heart failure publication-title: Basic Res Cardiol – volume: 28 start-page: 125 year: 2022 ident: bib23 article-title: SHP-1 knockdown suppresses mitochondrial biogenesis and aggravates mitochondria-dependent apoptosis induced by all trans retinal through the STING/AMPK pathways publication-title: Mol Med – volume: 485 start-page: 251 year: 2012 end-page: 255 ident: bib15 article-title: Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure publication-title: Nature – volume: 350 start-page: aad0116 year: 2015 ident: bib18 article-title: Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice publication-title: Science – volume: 561 start-page: 258 year: 2018 end-page: 262 ident: bib45 article-title: Parkin and PINK1 mitigate STING-induced inflammation publication-title: Nature – year: December 23, 2022 ident: bib5 article-title: Heart failure and ejection fraction publication-title: StatPearls. Treasure Island (FL): StatPearls Publishing – volume: 114 start-page: 12196 year: 2017 end-page: 12201 ident: bib16 article-title: DsbA-L prevents obesity-induced inflammation and insulin resistance by suppressing the mtDNA release-activated cGAS-cGAMP-STING pathway publication-title: Proc Natl Acad Sci U S A – volume: 13 start-page: 165 year: 2013 end-page: 172 ident: bib38 article-title: Oxidative stress and transforming growth factor-β1-induced cardiac fibrosis publication-title: Cardiovasc Hematol Disord: Drug Targets – volume: 114 start-page: 979 year: 2018 end-page: 991 ident: bib17 article-title: Enhancing fatty acid utilization ameliorates mitochondrial fragmentation and cardiac dysfunction via rebalancing optic atrophy 1 processing in the failing heart publication-title: Cardiovasc Res – volume: 37 start-page: 920 year: 2017 end-page: 929 ident: bib34 article-title: STING-IRF publication-title: Arterioscler Thromb Vasc Biol – volume: 594 start-page: 509 year: 2016 end-page: 525 ident: bib20 article-title: Mitochondrial dynamics, mitophagy and cardiovascular disease publication-title: J Physiol – volume: 93 start-page: 253 year: 2015 end-page: 262 ident: bib19 article-title: Mitophagy and heart failure publication-title: J Mol Med – volume: 28 start-page: R170 year: 2018 end-page: R185 ident: bib43 article-title: Mitophagy and quality control mechanisms in mitochondrial maintenance publication-title: Curr Biol – volume: 123 start-page: 594 year: 2011 end-page: 604 ident: bib32 article-title: Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury publication-title: Circulation – volume: 26 year: 2019 ident: bib22 article-title: PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation publication-title: Redox Biol – volume: 21 year: 2020 ident: bib14 article-title: Mitochondrial DNA in inflammation and immunity publication-title: EMBO Rep – volume: 102 start-page: 258 year: 2014 end-page: 269 ident: bib31 article-title: Crosstalk between fibroblasts and inflammatory cells publication-title: Cardiovasc Res – volume: 108 start-page: 9572 year: 2011 end-page: 9577 ident: bib26 article-title: PTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function publication-title: Proc Natl Acad Sci U S A – volume: 137 start-page: 2613 year: 2018 end-page: 2634 ident: bib8 article-title: Cytosolic DNA sensing promotes macrophage transformation and governs myocardial ischemic injury publication-title: Circulation – volume: 24 start-page: 1583 year: 2019 ident: bib40 article-title: Oxidative stress: a key modulator in neurodegenerative diseases publication-title: Molecules – volume: 339 start-page: 786 year: 2013 end-page: 791 ident: bib10 article-title: Cyclic GMP-AMP synthase is a cytosolic DNA sensor that activates the type I interferon pathway publication-title: Science – volume: 19 start-page: 109 year: 2021 ident: bib37 article-title: STING protects against cardiac dysfunction and remodelling by blocking autophagy publication-title: Cell Commun Signal – volume: 475 start-page: 839 year: 2018 end-page: 852 ident: bib11 article-title: Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases publication-title: Biochem J – volume: 105 start-page: 260 year: 2015 end-page: 270 ident: bib28 article-title: Functional crosstalk between cardiac fibroblasts and adult cardiomyocytes by soluble mediators publication-title: Cardiovasc Res – volume: 121 start-page: 575 year: 2017 end-page: 583 ident: bib29 article-title: Inhibition of the cardiac fibroblast-enriched lncRNA publication-title: Circ Res – volume: 19 start-page: 1379 issue: 11 year: 2017 ident: 10.1016/j.gendis.2023.08.003_bib4 article-title: Immune mechanisms in heart failure publication-title: Eur J Heart Fail doi: 10.1002/ejhf.942 – volume: 37 start-page: 920 issue: 5 year: 2017 ident: 10.1016/j.gendis.2023.08.003_bib34 article-title: STING-IRF3 triggers endothelial inflammation in response to free fatty acid-induced mitochondrial damage in diet-induced obesity publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.117.309017 – volume: 24 start-page: 1583 issue: 8 year: 2019 ident: 10.1016/j.gendis.2023.08.003_bib40 article-title: Oxidative stress: a key modulator in neurodegenerative diseases publication-title: Molecules doi: 10.3390/molecules24081583 – volume: 105 start-page: 260 issue: 3 year: 2015 ident: 10.1016/j.gendis.2023.08.003_bib28 article-title: Functional crosstalk between cardiac fibroblasts and adult cardiomyocytes by soluble mediators publication-title: Cardiovasc Res doi: 10.1093/cvr/cvu264 – volume: 141 start-page: 42 issue: 1 year: 2020 ident: 10.1016/j.gendis.2023.08.003_bib33 article-title: Critical role of cytosolic DNA and its sensing adaptor STING in aortic degeneration, dissection, and rupture publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.119.041460 – volume: 125 year: 2020 ident: 10.1016/j.gendis.2023.08.003_bib36 article-title: STING is an essential regulator of heart inflammation and fibrosis in mice with pathological cardiac hypertrophy via endoplasmic reticulum (ER) stress publication-title: Biomed Pharmacother doi: 10.1016/j.biopha.2020.110022 – volume: 121 start-page: 575 issue: 5 year: 2017 ident: 10.1016/j.gendis.2023.08.003_bib29 article-title: Inhibition of the cardiac fibroblast-enriched lncRNA Meg3 prevents cardiac fibrosis and diastolic dysfunction publication-title: Circ Res doi: 10.1161/CIRCRESAHA.117.310624 – volume: 114 start-page: 19 issue: 3 year: 2019 ident: 10.1016/j.gendis.2023.08.003_bib3 article-title: Inflammation and fibrosis in murine models of heart failure publication-title: Basic Res Cardiol doi: 10.1007/s00395-019-0722-5 – volume: 70 start-page: 74 year: 2014 ident: 10.1016/j.gendis.2023.08.003_bib25 article-title: Fibroblasts in myocardial infarction: a role in inflammation and repair publication-title: J Mol Cell Cardiol doi: 10.1016/j.yjmcc.2013.11.015 – volume: 561 start-page: 258 issue: 7722 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib45 article-title: Parkin and PINK1 mitigate STING-induced inflammation publication-title: Nature doi: 10.1038/s41586-018-0448-9 – volume: 26 year: 2019 ident: 10.1016/j.gendis.2023.08.003_bib22 article-title: PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation publication-title: Redox Biol doi: 10.1016/j.redox.2019.101254 – volume: 114 start-page: 979 issue: 7 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib17 article-title: Enhancing fatty acid utilization ameliorates mitochondrial fragmentation and cardiac dysfunction via rebalancing optic atrophy 1 processing in the failing heart publication-title: Cardiovasc Res doi: 10.1093/cvr/cvy052 – volume: 108 start-page: 9572 issue: 23 year: 2011 ident: 10.1016/j.gendis.2023.08.003_bib26 article-title: PTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1106291108 – volume: 15 start-page: 83 issue: 2 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib1 article-title: Reverse remodelling and myocardial recovery in heart failure publication-title: Nat Rev Cardiol doi: 10.1038/nrcardio.2017.139 – volume: 159 start-page: 1549 issue: 7 year: 2014 ident: 10.1016/j.gendis.2023.08.003_bib27 article-title: Apoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production publication-title: Cell doi: 10.1016/j.cell.2014.11.036 – volume: 19 start-page: 109 issue: 1 year: 2021 ident: 10.1016/j.gendis.2023.08.003_bib37 article-title: STING protects against cardiac dysfunction and remodelling by blocking autophagy publication-title: Cell Commun Signal doi: 10.1186/s12964-021-00793-0 – volume: 30 start-page: 784 issue: 4 year: 2019 ident: 10.1016/j.gendis.2023.08.003_bib41 article-title: Mitochondrial damage and activation of the STING pathway lead to renal inflammation and fibrosis publication-title: Cell Metabol doi: 10.1016/j.cmet.2019.08.003 – volume: 485 start-page: 251 issue: 7397 year: 2012 ident: 10.1016/j.gendis.2023.08.003_bib15 article-title: Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure publication-title: Nature doi: 10.1038/nature10992 – volume: 28 start-page: R170 issue: 4 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib43 article-title: Mitophagy and quality control mechanisms in mitochondrial maintenance publication-title: Curr Biol doi: 10.1016/j.cub.2018.01.004 – volume: 122 start-page: 712 issue: 5 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib21 article-title: AMPKα2 protects against the development of heart failure by enhancing mitophagy via PINK1 phosphorylation publication-title: Circ Res doi: 10.1161/CIRCRESAHA.117.312317 – volume: 339 start-page: 786 issue: 6121 year: 2013 ident: 10.1016/j.gendis.2023.08.003_bib10 article-title: Cyclic GMP-AMP synthase is a cytosolic DNA sensor that activates the type I interferon pathway publication-title: Science doi: 10.1126/science.1232458 – year: 2022 ident: 10.1016/j.gendis.2023.08.003_bib5 article-title: Heart failure and ejection fraction publication-title: StatPearls. Treasure Island (FL): StatPearls Publishing – volume: 475 start-page: 839 issue: 5 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib11 article-title: Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases publication-title: Biochem J doi: 10.1042/BCJ20170714 – volume: 5 start-page: 267 issue: 4 year: 2021 ident: 10.1016/j.gendis.2023.08.003_bib30 article-title: Myocardial fibrosis in the pathogenesis, diagnosis, and treatment of hypertrophic cardiomyopathy publication-title: Cardiovasc Innov Appl – volume: 131 start-page: 643 issue: 7 year: 2015 ident: 10.1016/j.gendis.2023.08.003_bib39 article-title: NADPH oxidase 4 induces cardiac fibrosis and hypertrophy through activating Akt/mTOR and NFκB signaling pathways publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.114.011079 – volume: 13 start-page: 165 issue: 2 year: 2013 ident: 10.1016/j.gendis.2023.08.003_bib38 article-title: Oxidative stress and transforming growth factor-β1-induced cardiac fibrosis publication-title: Cardiovasc Hematol Disord: Drug Targets doi: 10.2174/1871529X11313020010 – volume: 8 issue: 1 year: 2023 ident: 10.1016/j.gendis.2023.08.003_bib7 article-title: Inhibition of Stimulator of interferon genes protects against myocardial ischemia-reperfusion injury in diabetic mice publication-title: Cardiovasc Innov Appl – volume: 72 start-page: 1879 issue: 9 year: 2020 ident: 10.1016/j.gendis.2023.08.003_bib13 article-title: Pro-inflammatory role of cell-free mitochondrial DNA in cardiovascular diseases publication-title: IUBMB Life doi: 10.1002/iub.2339 – volume: 102 start-page: 258 issue: 2 year: 2014 ident: 10.1016/j.gendis.2023.08.003_bib31 article-title: Crosstalk between fibroblasts and inflammatory cells publication-title: Cardiovasc Res doi: 10.1093/cvr/cvu062 – volume: 17 start-page: 1142 issue: 10 year: 2016 ident: 10.1016/j.gendis.2023.08.003_bib9 article-title: Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing publication-title: Nat Immunol doi: 10.1038/ni.3558 – volume: 21 issue: 4 year: 2020 ident: 10.1016/j.gendis.2023.08.003_bib14 article-title: Mitochondrial DNA in inflammation and immunity publication-title: EMBO Rep doi: 10.15252/embr.201949799 – volume: 114 start-page: 12196 issue: 46 year: 2017 ident: 10.1016/j.gendis.2023.08.003_bib16 article-title: DsbA-L prevents obesity-induced inflammation and insulin resistance by suppressing the mtDNA release-activated cGAS-cGAMP-STING pathway publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.1708744114 – volume: 41 start-page: 2 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib44 article-title: Mitophagy and the release of inflammatory cytokines publication-title: Mitochondrion doi: 10.1016/j.mito.2017.10.009 – volume: 93 start-page: 253 issue: 3 year: 2015 ident: 10.1016/j.gendis.2023.08.003_bib19 article-title: Mitophagy and heart failure publication-title: J Mol Med doi: 10.1007/s00109-015-1254-6 – volume: 28 start-page: 125 issue: 1 year: 2022 ident: 10.1016/j.gendis.2023.08.003_bib23 article-title: SHP-1 knockdown suppresses mitochondrial biogenesis and aggravates mitochondria-dependent apoptosis induced by all trans retinal through the STING/AMPK pathways publication-title: Mol Med doi: 10.1186/s10020-022-00554-w – volume: 123 start-page: 594 issue: 6 year: 2011 ident: 10.1016/j.gendis.2023.08.003_bib32 article-title: Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.110.982777 – volume: 350 start-page: aad0116 issue: 6265 year: 2015 ident: 10.1016/j.gendis.2023.08.003_bib18 article-title: Imbalanced OPA1 processing and mitochondrial fragmentation cause heart failure in mice publication-title: Science doi: 10.1126/science.aad0116 – volume: 320 start-page: F608 issue: 4 year: 2021 ident: 10.1016/j.gendis.2023.08.003_bib24 article-title: The novel STING antagonist H151 ameliorates cisplatin-induced acute kidney injury and mitochondrial dysfunction publication-title: Am J Physiol Ren Physiol doi: 10.1152/ajprenal.00554.2020 – volume: 137 start-page: 2613 issue: 24 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib8 article-title: Cytosolic DNA sensing promotes macrophage transformation and governs myocardial ischemic injury publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.117.031046 – volume: 594 start-page: 509 issue: 3 year: 2016 ident: 10.1016/j.gendis.2023.08.003_bib20 article-title: Mitochondrial dynamics, mitophagy and cardiovascular disease publication-title: J Physiol doi: 10.1113/JP271301 – volume: 23 start-page: 1481 issue: 12 year: 2017 ident: 10.1016/j.gendis.2023.08.003_bib6 article-title: IRF3 and type I interferons fuel a fatal response to myocardial infarction publication-title: Nat Med doi: 10.1038/nm.4428 – volume: 118 start-page: 1021 issue: 6 year: 2016 ident: 10.1016/j.gendis.2023.08.003_bib2 article-title: Cardiac fibrosis: the fibroblast awakens publication-title: Circ Res doi: 10.1161/CIRCRESAHA.115.306565 – volume: 9 start-page: 536 year: 2018 ident: 10.1016/j.gendis.2023.08.003_bib12 article-title: Mitochondria: an organelle of bacterial origin controlling inflammation publication-title: Front Immunol doi: 10.3389/fimmu.2018.00536 – volume: 33 start-page: 817 issue: 4 year: 2014 ident: 10.1016/j.gendis.2023.08.003_bib42 article-title: Mitochondrial DNA induces inflammation and increases TLR9/NF-κB expression in lung tissue publication-title: Int J Mol Med doi: 10.3892/ijmm.2014.1650 – volume: 318 start-page: H1525 issue: 6 year: 2020 ident: 10.1016/j.gendis.2023.08.003_bib35 article-title: Cytosolic DNA sensor cGAS plays an essential pathogenetic role in pressure overload-induced heart failure publication-title: Am J Physiol Heart Circ Physiol doi: 10.1152/ajpheart.00097.2020 |
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