Exogenous SDF-1α Protects Human Myocardium from Hypoxia-Reoxygenation Injury via CXCR4

A. Malik, Daniel Ian Bromage, Zhenhe He, Luciano Candilio, A Hamarneh, Stasa Taferner, Sean M Davidson, Derek M. Yellon

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


ST-segment elevation myocardial infarction (STEMI) is a consequence of atherosclerotic plaque rupture and thrombotic occlusion of the coronary artery causing downstream ischaemia and, eventually, cell death. The most effective therapeutic strategy for STEMI is timely reperfusion by primary percutaneous coronary intervention (PPCI). Such reperfusion is a prerequisite for myocardial salvage, leading to smaller infarct sizes and improved clinical outcomes [1, 2]. However, reperfusion can itself inflict further injury, termed ischaemia-reperfusion injury (IRI). Despite PPCI, a recent study found 30-day, 1-year, and 5-year mortality following STEMI to be 7.9 %, 11.4 %, and 23.3 %, respectively [3]. Consequently, novel strategies to mitigate the deleterious effects of IRI are paramount.

Stromal derived factor-1α (SDF-1α or CXCL12) is a chemokine that has demonstrated cardioprotective activity in mice [4]. We recently demonstrated that exogenous SDF-1α improved functional recovery of ex vivo rat cardiac papillary muscle subjected to hypoxia and reoxygenation (simulated IRI) [5]. This effect was abrogated by pre-treatment with AMD3100, a highly specific antagonist of the SDF-1α receptor, CXCR4.

However, it is not known whether SDF-1α can similarly protect human heart tissue and whether any such protection is afforded via CXCR4. We address this question using isolated human atrial trabeculae subjected to simulated IRI.
Original languageEnglish
JournalCardiovascular Drugs and Therapy
Publication statusPublished - 20 Oct 2015


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