Use of Multifactorial Treatments to Address the Challenge of Translating Experimental Myocardial Infarct Reduction Strategies

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  Figure 1. Literature search on Pubmed for the terms related to cardiac ischemia tissue injury show 16,752 publications since 1978. Search details: (“heart”[MeSH Terms] OR “heart”[All Fields] OR “cardiac”[All Fields]) OR (“ischaemia”[All Fields] OR “ischemia”[MeSH Terms] OR “ischemia”[All Fields]) OR (“tissues”[MeSH Terms] OR “tissues”[All Fields] OR “tissue”[All Fields]) OR (“wounds and injuries”[MeSH Terms] OR (“wounds”[All Fields] AND “injuries”[All Fields]) OR “wounds and injuries”[All Fields] OR “injury”[All Fields]) AND (“1978/01/01”[PDAT]: “2018/11/29”[PDAT]): https://www.ncbi.nlm.nih.gov/pubmed/; site visited on 29 November 2018.

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  Figure 2. Potential Mechanisms of EA1-Fc Mediated Cardioprotection. Treatment with Ephrin A1-Fc (EA1-Fc) in a mouse model of myocardial infarction (MI) was shown to alter expression of five Ephrin receptors (EphA1-A4 and EphA6) as well as endogenous EA1 ligand when compared to the vehicle treated MI group. Canonical ephrin signaling regulates a wide-variety of physiological processes. The cardioprotective role of EA1-Fc may be attributed to ephrin signaling. In support of this, in the EA1-Fc MI group, indicators of decreased apoptosis, increased autophagy, and decreased inflammation were observed. The possibility also exists that EA1-Fc injection is cardioprotective through a mechanism that is not normally attributed to ephrin signaling.

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  Figure 3. Comparison of pharmacological cardioprotective strategies’ efficacy to reduce infarct size due to ischemia/reperfusion injury [106].