Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure
Heart failure, a leading driver of global mortality, remains a topic of intense contemporary research interest due to the prevailing unmet need in cardiometabolic therapeutics. Numerous mechanisms with the potential to influence the onset and development of heart failure remain incompletely understo...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | Autophagy Reports |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/27694127.2024.2320605 |
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| author | Jialing Tang Eddie Tam Erfei Song Aimin Xu Gary Sweeney |
| author_facet | Jialing Tang Eddie Tam Erfei Song Aimin Xu Gary Sweeney |
| author_sort | Jialing Tang |
| collection | DOAJ |
| description | Heart failure, a leading driver of global mortality, remains a topic of intense contemporary research interest due to the prevailing unmet need in cardiometabolic therapeutics. Numerous mechanisms with the potential to influence the onset and development of heart failure remain incompletely understood. Firstly, myocardial autophagy, which involves lysosomal degradation of damaged cellular components, confers context-dependent beneficial and detrimental effects. Secondly, sterile inflammation may arise following cardiac stress and exacerbate the progression of heart failure. Inflammation changes in a temporal manner and its onset must be adequately resolved to limit progression of heart failure. Mitochondria are an important factor in contributing to sterile inflammation by releasing damage associated molecular patterns (DAMPs) including mitochondrial DNA (mtDNA). Accordingly, this is one reason why the selective autophagy of mitochondria to maintain optimal function is important in determining cardiac function. In this review, we examine the increasing evidence suggesting crosstalk between autophagy and sterile inflammation together with their role in the development of heart failure. In particular, this is exemplified in the preclinical models of ischaemia/reperfusion injury and pressure overload induced heart failure. We also highlight potential therapeutic approaches focusing on autophagy and addressing sterile inflammation, aiming to enhance outcomes in heart failure. |
| format | Article |
| id | doaj-art-7924a5ec7a0b46bf9182d15a49b41aa3 |
| institution | Kabale University |
| issn | 2769-4127 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Autophagy Reports |
| spelling | doaj-art-7924a5ec7a0b46bf9182d15a49b41aa32024-12-09T07:19:32ZengTaylor & Francis GroupAutophagy Reports2769-41272024-12-013110.1080/27694127.2024.2320605Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failureJialing Tang0Eddie Tam1Erfei Song2Aimin Xu3Gary Sweeney4Department of Biology, York University, Toronto, ON, CanadaDepartment of Biology, York University, Toronto, ON, CanadaDepartment of Medicine, School of Clinical Medicine, State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong KongDepartment of Medicine, School of Clinical Medicine, State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong KongDepartment of Biology, York University, Toronto, ON, CanadaHeart failure, a leading driver of global mortality, remains a topic of intense contemporary research interest due to the prevailing unmet need in cardiometabolic therapeutics. Numerous mechanisms with the potential to influence the onset and development of heart failure remain incompletely understood. Firstly, myocardial autophagy, which involves lysosomal degradation of damaged cellular components, confers context-dependent beneficial and detrimental effects. Secondly, sterile inflammation may arise following cardiac stress and exacerbate the progression of heart failure. Inflammation changes in a temporal manner and its onset must be adequately resolved to limit progression of heart failure. Mitochondria are an important factor in contributing to sterile inflammation by releasing damage associated molecular patterns (DAMPs) including mitochondrial DNA (mtDNA). Accordingly, this is one reason why the selective autophagy of mitochondria to maintain optimal function is important in determining cardiac function. In this review, we examine the increasing evidence suggesting crosstalk between autophagy and sterile inflammation together with their role in the development of heart failure. In particular, this is exemplified in the preclinical models of ischaemia/reperfusion injury and pressure overload induced heart failure. We also highlight potential therapeutic approaches focusing on autophagy and addressing sterile inflammation, aiming to enhance outcomes in heart failure.https://www.tandfonline.com/doi/10.1080/27694127.2024.2320605Autophagysterile inflammationheart failureischaemia/reperfusionpressure overload |
| spellingShingle | Jialing Tang Eddie Tam Erfei Song Aimin Xu Gary Sweeney Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure Autophagy Reports Autophagy sterile inflammation heart failure ischaemia/reperfusion pressure overload |
| title | Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure |
| title_full | Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure |
| title_fullStr | Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure |
| title_full_unstemmed | Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure |
| title_short | Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure |
| title_sort | crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure |
| topic | Autophagy sterile inflammation heart failure ischaemia/reperfusion pressure overload |
| url | https://www.tandfonline.com/doi/10.1080/27694127.2024.2320605 |
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