ORIGINAL RESEARCH article
Front. Immunol.
Sec. Molecular Innate Immunity
SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism
Provisionally accepted
- 1The First Hospital of Jilin University, Changchun, China
- 2Jilin Province Cancer Hospital, Changchun, China
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Solute carrier family 31 member 1 (SLC31A1) has demonstrated strong diagnostic value in heart failure (HF) due to its link with energy metabolism and immune activity. This study aimed to explore its therapeutic potential in post-acute myocardial infarction (AMI) HF. SLC31A1 was highly expressed in macrophages of post-AMI HF mice, while its knockdown via shRNA inhibited cardiomyocyte apoptosis and delayed HF progression. Mechanistically, SLC31A1 knockdown modulated copper metabolism, reduced macrophage cuproptosis and HMGB1 release, and suppressed inflammatory responses through NLRP3 inflammasome inactivation. Similarly, the copper chelator ATTM alleviated inflammation and cardiomyocyte injury, confirming in vitro findings. Notably, NLRP3/HMGB1 pathway activation partially reversed the protective effects of SLC31A1 silencing. These results reveal a novel role of SLC31A1 in regulating cuproptosis and inflammation in post-AMI HF, suggesting it as a promising therapeutic target.
Keywords: acute myocardial infarction, Apoptosis, Copper metabolism, cuproptosis, Heart Failure, HMGB1, Macrophages, NLRP3
Received: 17 Sep 2025; Accepted: 12 Jan 2026.
Copyright: © 2026 Wei, Qin, Sun and Zhou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Huanyu Zhou
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