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. 2022 Jul 7;13:36. doi: 10.1186/s13293-022-00446-y

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© The Author(s) 2022

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. 8 — Effect of cigarette smoke (CS) on IL-6 and TNF-α proinflammatory markers fold change at day 7 post-MI. A CS-exposed MI male group had greater IL-6 mRNA expression levels compared to CS-naive MI males. Female groups had comparable IL-6 mRNA expression levels post-MI irrespective of smoke exposure. No difference across sexes was observed (B) CS-exposed MI male group had greater TNF-α mRNA expression levels compared to control males and CS-exposed MI female group. Female groups had comparable TNF-α mRNA expression levels post-MI irrespective of smoke exposure. N = 3 in each group. CTL control, MI myocardial infarction, MICS smoking plus MI. *p < 0.05; ANOVA