TRPM7 mediates endoplasmic reticulum stress and ferroptosis in sepsis-induced myocardial injury
Abstract Transient receptor potential melastatin 7 (TRPM7), a non-selective cation channel, was significantly upregulated in the blood of patients with sepsis. This study focuses on the preliminary exploration of the probable regulatory mechanism of TRPM7 in sepsis-induced myocardial injury (SIMI). HL-1 cardiac muscle cell line was treated with lipopolysaccharide (LPS) to mimic SIMI in vitro, and TRPM7 level was assessed. The impacts of TRPM7 knockdown on cellular inflammation response, oxidative stress, apoptosis, endoplasmic reticulum (ER) stress, and ferroptosis were identified. In order to explore the mechanism, ER stress agonist tunicamycin (TM) or ferroptosis inducer erastin was applied to treat HL-1 cells. The influences of TM and erastin on the aforementioned aspects were evaluated. TRPM7 was elevated in response to LPS stimulation, and its knockdown reduced the secretion of inflammatory factors and oxidative stress degree. Moreover, TRPM7 knockdown significantly suppressed cell apoptosis, ER stress, and ferroptosis. TM and erastin reversed the functions of TRPM7 knockdown, indicating ER stress and ferroptosis mediated in the regulation of TRPM7. This research proposes the possibility of TRPM7 as a marker or target for SIMI, and provides theoretical support for follow-up research..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:55 |
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| Enthalten in: |
Journal of bioenergetics and biomembranes - 55(2023), 3 vom: Juni, Seite 207-217 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Deng, Wenlong [VerfasserIn] |
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| Links: |
Volltext [lizenzpflichtig] |
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| Themen: |
Cardiac muscle cell |
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| Anmerkungen: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| doi: |
10.1007/s10863-023-09968-5 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Abstract Transient receptor potential melastatin 7 (TRPM7), a non-selective cation channel, was significantly upregulated in the blood of patients with sepsis. This study focuses on the preliminary exploration of the probable regulatory mechanism of TRPM7 in sepsis-induced myocardial injury (SIMI). HL-1 cardiac muscle cell line was treated with lipopolysaccharide (LPS) to mimic SIMI in vitro, and TRPM7 level was assessed. The impacts of TRPM7 knockdown on cellular inflammation response, oxidative stress, apoptosis, endoplasmic reticulum (ER) stress, and ferroptosis were identified. In order to explore the mechanism, ER stress agonist tunicamycin (TM) or ferroptosis inducer erastin was applied to treat HL-1 cells. The influences of TM and erastin on the aforementioned aspects were evaluated. TRPM7 was elevated in response to LPS stimulation, and its knockdown reduced the secretion of inflammatory factors and oxidative stress degree. Moreover, TRPM7 knockdown significantly suppressed cell apoptosis, ER stress, and ferroptosis. TM and erastin reversed the functions of TRPM7 knockdown, indicating ER stress and ferroptosis mediated in the regulation of TRPM7. This research proposes the possibility of TRPM7 as a marker or target for SIMI, and provides theoretical support for follow-up research. | ||
| 650 | 4 | |a Transient receptor potential melastatin 7 | |
| 650 | 4 | |a Sepsis-induced myocardial injury | |
| 650 | 4 | |a Endoplasmic reticulum stress | |
| 650 | 4 | |a Ferroptosis | |
| 650 | 4 | |a Cardiac muscle cell | |
| 700 | 1 | |a Ren, Guobin |4 aut | |
| 700 | 1 | |a Luo, Jiajing |4 aut | |
| 700 | 1 | |a Gao, She |4 aut | |
| 700 | 1 | |a Huang, Weihong |4 aut | |
| 700 | 1 | |a Liu, Weitao |4 aut | |
| 700 | 1 | |a Ye, Shupei |4 aut | |
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