JZUS - Journal of Zhejiang University SCIENCE

Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

IL-15 aggravates cardiac ischemia injury via impairing macrophage efferocytosis and driving inflammation

Author(s): Lei GUO^1, ^2, ^3, ^4, Zhehui YIN^1, ^2, ^3, Ning ZHANG5⁵, Han CHEN^1, ^2, ³, Zhuo WANG^1, ^2, ³, Yuxue HUANG⁷, Jiniu HUANG^1, ^2, ³, Yayu YOU⁶, Chenyun ZHANG^1, ^2, ³, Qinyi BAO^1, ^2, ³, Shuxin LEI^1, ^2, ³, Jun JIANG^1, ^2, ³, Xiaojie XIE^1, ^2, ³
Affiliation(s): ¹Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China ²State Key Laboratory of Transvascular Implantation Devices, Hangzhou 310009, China ³Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou 310009, China ⁴Department of General Practice and International Medicine, Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China ⁵Department of Cardiology, Hangzhou First Affiliated People's Hospital, Westlake University School of Medicine, Hangzhou 310003, China ⁶Department of Cardiology, Hunan Provincial People's Hospital, Changsha 410000, Hunan, China ⁷Department of Cardiology, First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
Corresponding email(s): Xiaojie XIE, xiexj@zju.edu.cn Jun JIANG, 2106002@zju.edu.cn
Key Words: Myocardial infarction, Inflammatory phenotype, Macrophage function, Metabolic reprogramming, Interleukin-15 (IL-15)

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Lei GUO^1,^2,^3,^4*, Zhehui YIN^1,^2,^3*, Ning ZHANG5⁵, Han CHEN^1,^2,³, Zhuo WANG^1,^2,³, Yuxue HUANG⁷, Jiniu HUANG^1,^2,³, Yayu YOU⁶, Chenyun ZHANG^1,^2,³, Qinyi BAO^1,^2,³, Shuxin LEI^1,^2,³, Jun JIANG^1,^2,³, Xiaojie XIE^1,^2,³. IL-15 aggravates cardiac ischemia injury via impairing macrophage efferocytosis and driving inflammation[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

@article{title="IL-15 aggravates cardiac ischemia injury via impairing macrophage efferocytosis and driving inflammation",
author="Lei GUO^1,^2,^3,^4*, Zhehui YIN^1,^2,^3*, Ning ZHANG5⁵, Han CHEN^1,^2,³, Zhuo WANG^1,^2,³, Yuxue HUANG⁷, Jiniu HUANG^1,^2,³, Yayu YOU⁶, Chenyun ZHANG^1,^2,³, Qinyi BAO^1,^2,³, Shuxin LEI^1,^2,³, Jun JIANG^1,^2,³, Xiaojie XIE^1,^2,³",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2500477"
}

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Abstract
Chinese Summary
Academic Network
Reviewer Comment

Abstract: Acute myocardial infarction (AMI) remains a major global health burden, which is characterized by profound cardiac inflammation, apoptotic cell death, and impaired myocardial function. While interleukin-15 (IL-15) has been implicated in immune regulation, its precise role in the pathogenesis of AMI has not been clarified. Therefore, this study sought to delineate the functional role of IL-15 in the progression of AMI, with a particular focus on its influence on macrophage-driven inflammation, efferocytosis, and metabolic reprogramming. IL-15 levels were assessed in AMI patients and murine models. To evaluate the impact of IL-15 on cardiac inflammation, apoptosis, and functional outcomes following AMI, IL-15 and interleukin-15 receptor (IL-15R) α knockout (KO) mouse models were employed. Mechanistic studies were conducted to investigate IL-15-mediated effects on macrophage efferocytosis, polarization and metabolic remodeling, with an emphasis on nuclear factor kappa-B (NF-ΚB) signaling and glycolytic flux. Elevated IL-15 levels were detected in both the plasma of AMI patients and the cardiac tissues of murine AMI models, correlating with increased disease severity. The genetic deletion of IL-15 or IL-15Rα significantly ameliorated cardiac injury by reducing inflammation and apoptosis while preserving myocardial function. Mechanistic analyses revealed that IL-15 impaired macrophage efferocytosis via MERTK downregulation and promoted M1 polarization via NF-ΚB pathway activation. Furthermore, IL-15 reprogrammed macrophage metabolism by enhancing glycolytic activity. Ultimately, IL-15 restoration exacerbated cardiac ischemia injury following AMI, serving as a critical regulator of macrophage-mediated inflammation in AMI. These findings highlight the role of IL-15 as a potential therapeutic and prognostic target for mitigating cardiac inflammation and improving myocardial recovery in AMI

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