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. 2023 Feb 6;44(8):1612–1624. doi: 10.1038/s41401-023-01059-w

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© The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society 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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Fig. 8 — Schematic cartoon illustrating the protective mechanism of SCN ablation against MI in mice: the increased expression of IGF2 in SCNx mice promotes localized resting macrophage transition into anti-inflammatory macrophages in the heart and eventually preserves cardiac function by promoting angiogenesis and inhibiting fibrosis in the infarcted heart.