Data on necrotic and apoptotic cell death in acute myocardial ischemia/reperfusion injury: the effects of CaMKII and angiotensin AT1 receptor inhibition

Tomas Rajtik; Slavka Carnicka; Adrian Szobi; Zoltan Giricz; Jin O-Uchi; Veronika Hassova; Pavel Svec; Peter Ferdinandy; Tanya Ravingerova; Adriana Adameova

doi:10.1016/j.dib.2016.03.017

Data on necrotic and apoptotic cell death in acute myocardial ischemia/reperfusion injury: the effects of CaMKII and angiotensin AT1 receptor inhibition

Data Brief. 2016 Mar 10:7:730-4. doi: 10.1016/j.dib.2016.03.017. eCollection 2016 Jun.

Authors

Affiliations

¹ Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, Slovak Republic.
² Institute for Heart Research, Slovak Academy of Sciences & Centre of Excellence, SAS NOREG, Bratislava, Slovak Republic.
³ Cardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
⁴ Department of Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, USA.
⁵ Cardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; PharmaHungary Group, Szeged, Hungary.

Abstract

Content of particular proteins indicating cellular injury due to apoptosis and necrosis has been investigated in ischemic/reperfused (IR) hearts and ischemic/reperfused hearts treated with CaMKII inhibitor and/or AT1 receptor inhibitor. This data article provides information in support of the original research article "Oxidative activation of CaMKIIδ in acute myocardial ischemia/reperfusion injury: a role of angiotensin AT1 receptor-NOX2 signaling axis" [1].

Keywords: AT1 receptor blockade; Apoptosis; CaMKII inhibition; Myocardial ischemia/reperfusion injury; Necrosis.