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editorial

. 2020 Jun 12;115(4):44. doi: 10.1007/s00395-020-0801-7

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© The Author(s) 2020

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/.

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Fig. 1 — Scheme illustrating the mechanisms of cardioprotection by nitric oxide or the aggravation of ischemic cardiac damage by impaired nitric oxide signaling. Nitric oxide confers known cardioprotective effects and attenuates I/R cardiac damage (as observed in STEMI and NSTEMI [17]). The protective effects are lost by genetic or pharmacological eNOS inhibition. Implications for the novel findings on interplay of red blood cell/vascular eNOS for cardioprotection in a model of anemia are described [28]. In principle, anemic patients have a worse prognosis after AMI or ACS due to dysfunctional RBC ^·NO signaling, but upregulation of eNOS activity in the heart and vessels of anemic patients provides compensatory protection that is lost upon genetic or pharmacological eNOS inhibition. GTPCH-1 GTP-cyclohydrolase-1, GTN glycerol trinitrate (nitroglycerin), STEMI ST-elevation myocardial infarction, NSTEMI non-STEMI. Contains images from Servier Medical Art by Servier, licensed under a Creative Commons Attribution 3.0 Unported License