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. 2021 Feb 26;15:15. doi: 10.1186/s40246-021-00314-7

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — CXCL16 expression was elevated in MI and human neonatal cardiomyocytes in response to H/R treatment. a GSEA analysis was applied to detect the correction between chemokine-related genes and MI. b The Venn curve exhibited that there are two overlapped differentially expressed genes: CXCL16 and NCF1. Blue represents the DEGs obtained from the GEO database and yellow represents the upregulated chemokine genes in MI. c Relative expression of CXCL16 in MI tissues (n = 17) and normal specimens (n = 7) based on the GSE60993, P = 0.0019. d Relative expression of CXCL16 in human neonatal cardiomyocytes evoked by the H/R and control group, **P < 0.01 vs. control. n = 3 independent experiments. All data were exhibited as mean ± standard deviation (SD)