The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome
Abstract Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe respiratory condition associated with elevated morbidity and mortality. Understanding their complex pathophysiological mechanisms is crucial for developing new preventive and therapeutic strategies. Recent studie...
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| Language: | English |
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Wiley
2024-12-01
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| Series: | Clinical and Translational Medicine |
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| Online Access: | https://doi.org/10.1002/ctm2.70098 |
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| author | Lan Luo Xiaoli Zhuang Lin Fu Ziyuan Dong Shuyuan Yi Kan Wang Yu Jiang Ju Zhao Xiaofang Yang Feilong Hei |
| author_facet | Lan Luo Xiaoli Zhuang Lin Fu Ziyuan Dong Shuyuan Yi Kan Wang Yu Jiang Ju Zhao Xiaofang Yang Feilong Hei |
| author_sort | Lan Luo |
| collection | DOAJ |
| description | Abstract Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe respiratory condition associated with elevated morbidity and mortality. Understanding their complex pathophysiological mechanisms is crucial for developing new preventive and therapeutic strategies. Recent studies highlight the significant role of inflammation involved in ALI/ARDS, particularly the hyperactivation of the NOD‐like receptor thermal protein domain‐associated protein 3 (NLRP3) inflammasome in macrophages. This activation drives pulmonary inflammation by releasing inflammatory signalling molecules and is linked to metabolic reprogramming, marked by increased glycolysis and reduced oxidative phosphorylation. However, the relationship between NLRP3 inflammasome activation and macrophage glycolytic reprogramming in ALI/ARDS, as well as the molecular mechanisms regulating these processes, remain elusive. This review provides a detailed description of the interactions and potential mechanisms linking NLRP3 inflammasome activation with macrophage glycolytic reprogramming, proposing that glycolytic reprogramming may represent a promising therapeutic target for mitigating inflammatory responses in ALI/ARDS. Key points NLRP3 inflammasome activation is pivotal in mediating the excessive inflammatory response in ALI/ARDS. Glycolytic reprogramming regulates NLRP3 inflammasome activation. Therapeutic potential of targeting glycolytic reprogramming to inhibit NLRP3 inflammasome activation in ALI/ARDS. |
| format | Article |
| id | doaj-art-d30dad2259ae4c6f923c09365dc100fb |
| institution | Kabale University |
| issn | 2001-1326 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Wiley |
| record_format | Article |
| series | Clinical and Translational Medicine |
| spelling | doaj-art-d30dad2259ae4c6f923c09365dc100fb2025-01-30T03:56:54ZengWileyClinical and Translational Medicine2001-13262024-12-011412n/an/a10.1002/ctm2.70098The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndromeLan Luo0Xiaoli Zhuang1Lin Fu2Ziyuan Dong3Shuyuan Yi4Kan Wang5Yu Jiang6Ju Zhao7Xiaofang Yang8Feilong Hei9Department of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaDepartment of Extracorporeal Circulation and Mechanical Circulation Assistants Center for Cardiac Intensive Care Beijing Anzhen Hospital Capital Medical University Beijing ChinaAbstract Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a severe respiratory condition associated with elevated morbidity and mortality. Understanding their complex pathophysiological mechanisms is crucial for developing new preventive and therapeutic strategies. Recent studies highlight the significant role of inflammation involved in ALI/ARDS, particularly the hyperactivation of the NOD‐like receptor thermal protein domain‐associated protein 3 (NLRP3) inflammasome in macrophages. This activation drives pulmonary inflammation by releasing inflammatory signalling molecules and is linked to metabolic reprogramming, marked by increased glycolysis and reduced oxidative phosphorylation. However, the relationship between NLRP3 inflammasome activation and macrophage glycolytic reprogramming in ALI/ARDS, as well as the molecular mechanisms regulating these processes, remain elusive. This review provides a detailed description of the interactions and potential mechanisms linking NLRP3 inflammasome activation with macrophage glycolytic reprogramming, proposing that glycolytic reprogramming may represent a promising therapeutic target for mitigating inflammatory responses in ALI/ARDS. Key points NLRP3 inflammasome activation is pivotal in mediating the excessive inflammatory response in ALI/ARDS. Glycolytic reprogramming regulates NLRP3 inflammasome activation. Therapeutic potential of targeting glycolytic reprogramming to inhibit NLRP3 inflammasome activation in ALI/ARDS.https://doi.org/10.1002/ctm2.70098acute lung injury/acute respiratory distress syndromeglycolytic reprogrammingmacrophageNLRP3 inflammasome |
| spellingShingle | Lan Luo Xiaoli Zhuang Lin Fu Ziyuan Dong Shuyuan Yi Kan Wang Yu Jiang Ju Zhao Xiaofang Yang Feilong Hei The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome Clinical and Translational Medicine acute lung injury/acute respiratory distress syndrome glycolytic reprogramming macrophage NLRP3 inflammasome |
| title | The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome |
| title_full | The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome |
| title_fullStr | The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome |
| title_full_unstemmed | The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome |
| title_short | The role of the interplay between macrophage glycolytic reprogramming and NLRP3 inflammasome activation in acute lung injury/acute respiratory distress syndrome |
| title_sort | role of the interplay between macrophage glycolytic reprogramming and nlrp3 inflammasome activation in acute lung injury acute respiratory distress syndrome |
| topic | acute lung injury/acute respiratory distress syndrome glycolytic reprogramming macrophage NLRP3 inflammasome |
| url | https://doi.org/10.1002/ctm2.70098 |
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