Novel targets and future strategies for acute cardioprotection: Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart

Hausenloy, DJ ✉; Garcia-Dorado, D*; Erik, Botker H; Davidson, SM; Downey, J; Engel, FB; Jennings, R; Lecour, S; Leor, J; Madonna, R; Ovize, M; Perrino, C; Prunier, F; Schulz, R; Sluijter, JP; Van, Laake LW; Vinten-Johansen, J; Yellon, DM; Ytrehus, K; Heusch, G**; Ferdinandy, P ✉ [Ferdinandy, Péter (Farmakológia, mol...), szerző] Farmakológiai és Farmakoterápiás Intézet (SE / AOK / I)

Angol nyelvű Összefoglaló cikk (Folyóiratcikk) Tudományos
Megjelent: CARDIOVASCULAR RESEARCH 0008-6363 1755-3245 113 (6) pp. 564-585 2017
  • SJR Scopus - Cardiology and Cardiovascular Medicine: D1
  • Általános orvostudomány
  • Biológiai tudományok
  • Klinikai orvostan
Ischaemic heart disease and the heart failure that often results, remain the leading causes of death and disability in Europe and worldwide. As such, in order to prevent heart failure and improve clinical outcomes in patients presenting with an acute ST-segment elevation myocardial infarction and patients undergoing coronary artery bypass graft surgery, novel therapies are required to protect the heart against the detrimental effects of acute ischaemia/reperfusion injury. During the last three decades, a wide variety of ischaemic conditioning strategies and pharmacological treatments have been tested in the clinic - however, their translation from experimental to clinical studies for improving patient outcomes has been both challenging and disappointing. Therefore, in this Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart, we critically analyse the current state of ischaemic conditioning in both the experimental and clinical settings, provide recommendations for improving its translation into the clinical setting, and highlight novel therapeutic targets and new treatment strategies for reducing acute myocardial ischaemia/reperfusion injury.
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2024-07-14 18:11