Cardiac Metabolism in Sepsis
The mechanism of sepsis-induced cardiac dysfunction is believed to be different from that of myocardial ischemia. In sepsis, chemical mediators, such as endotoxins, cytokines, and nitric oxide, cause metabolic abnormalities, mitochondrial dysfunction, and downregulation of β-adrenergic receptors. Th...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-12-01
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| Series: | Metabolites |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2218-1989/11/12/846 |
| _version_ | 1827671207577649152 |
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| author | Satoshi Kawaguchi Motoi Okada |
| author_facet | Satoshi Kawaguchi Motoi Okada |
| author_sort | Satoshi Kawaguchi |
| collection | DOAJ |
| description | The mechanism of sepsis-induced cardiac dysfunction is believed to be different from that of myocardial ischemia. In sepsis, chemical mediators, such as endotoxins, cytokines, and nitric oxide, cause metabolic abnormalities, mitochondrial dysfunction, and downregulation of β-adrenergic receptors. These factors inhibit the production of ATP, essential for myocardial energy metabolism, resulting in cardiac dysfunction. This review focuses on the metabolic changes in sepsis, particularly in the heart. In addition to managing inflammation, interventions focusing on metabolism may be a new therapeutic strategy for cardiac dysfunction due to sepsis. |
| first_indexed | 2024-03-10T03:34:52Z |
| format | Article |
| id | doaj.art-136369af9fd74ba6930bb1bd32441eff |
| institution | Directory Open Access Journal |
| issn | 2218-1989 |
| language | English |
| last_indexed | 2024-03-10T03:34:52Z |
| publishDate | 2021-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Metabolites |
| spelling | doaj.art-136369af9fd74ba6930bb1bd32441eff2023-11-23T09:31:45ZengMDPI AGMetabolites2218-19892021-12-01111284610.3390/metabo11120846Cardiac Metabolism in SepsisSatoshi Kawaguchi0Motoi Okada1Department of Anatomy, Cell Biology and Physiology, Indiana University School of Medicine, Bloomington, IN 46202, USADepartment of Emergency Medicine, Asahikawa Medical University, Asahikawa 078-8510, JapanThe mechanism of sepsis-induced cardiac dysfunction is believed to be different from that of myocardial ischemia. In sepsis, chemical mediators, such as endotoxins, cytokines, and nitric oxide, cause metabolic abnormalities, mitochondrial dysfunction, and downregulation of β-adrenergic receptors. These factors inhibit the production of ATP, essential for myocardial energy metabolism, resulting in cardiac dysfunction. This review focuses on the metabolic changes in sepsis, particularly in the heart. In addition to managing inflammation, interventions focusing on metabolism may be a new therapeutic strategy for cardiac dysfunction due to sepsis.https://www.mdpi.com/2218-1989/11/12/846sepsisSICMβ-adrenergic receptormetabolic switchATP |
| spellingShingle | Satoshi Kawaguchi Motoi Okada Cardiac Metabolism in Sepsis Metabolites sepsis SICM β-adrenergic receptor metabolic switch ATP |
| title | Cardiac Metabolism in Sepsis |
| title_full | Cardiac Metabolism in Sepsis |
| title_fullStr | Cardiac Metabolism in Sepsis |
| title_full_unstemmed | Cardiac Metabolism in Sepsis |
| title_short | Cardiac Metabolism in Sepsis |
| title_sort | cardiac metabolism in sepsis |
| topic | sepsis SICM β-adrenergic receptor metabolic switch ATP |
| url | https://www.mdpi.com/2218-1989/11/12/846 |
| work_keys_str_mv | AT satoshikawaguchi cardiacmetabolisminsepsis AT motoiokada cardiacmetabolisminsepsis |