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. 2020 Jun 9;11:872. doi: 10.3389/fphar.2020.00872

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Copyright © 2020 Wang, Wang, He, Sun and Sun

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Calcium overload is the important target of treating myocardial ischemia/reperfusion (MI/R) injury. The maintenance of calcium homeostasis requires the participation of multiple regulatory proteins including LTCC, RyR2, SERCA, NCX, PLB, FKBP12.6, and CaMK II. When MI/R occurs, calcium homeostasis will be broken and further developed into calcium overload. Calcium overload further exacerbates MI/R injury. Therefore, inhibiting calcium overload is an effective way to reduce MI/R injury. These drugs currently on the market or under investigation including adenosine, ridogrel, vorapaxar, metoprolol, flunarizine, and zoniporide hydrochloride, are for the treatment of MI/R injury or have the potential to treat MI/R injury. These drugs can play a cardioprotective role by regulating the calcium signaling pathway.