TY - JOUR
T1 - Cardioprotection in ischaemia-reperfusion injury
T2 - Novel mechanisms and clinical translation
AU - Altamirano, Francisco
AU - Wang, Zhao
AU - Hill, Joseph A
N1 - Funding Information:
This work was supported by grants from the NIH (HL‐120732; HL‐100401), the American Heart Association (AHA) (14SFRN20510023; 14SFRN20670003), Fondation Leducq (11CVD04) and the Cancer Prevention and Research Institute of Texas (CPRIT) (RP110486P3). Z. V. Wang was supported by a Scientist Development Grant from the AHA (14SDG18440002).
Publisher Copyright:
© 2015 The Physiological Society.
PY - 2015/9/1
Y1 - 2015/9/1
N2 - In recent decades, robust successes have been achieved in conquering the acutely lethal manifestations of heart disease. Nevertheless, the prevalence of heart disease, especially heart failure, continues to rise. Among the precipitating aetiologies, ischaemic disease is a leading cause of heart failure. In the context of ischaemia, the myocardium is deprived of oxygen and nutrients, which elicits a cascade of events that provokes cell death. This ischaemic insult is typically coupled with reperfusion, either spontaneous or therapeutically imposed, wherein blood supply is restored to the previously ischaemic tissue. While this intervention limits ischaemic injury, it triggers a new cascade of events that is also harmful, viz. reperfusion injury. In recent years, novel insights have emerged regarding mechanisms of ischaemia-reperfusion injury, and some hold promise as targets of therapeutic relevance. Here, we review a select number of these pathways, focusing on recent discoveries and highlighting prospects for therapeutic manipulation for clinical benefit.
AB - In recent decades, robust successes have been achieved in conquering the acutely lethal manifestations of heart disease. Nevertheless, the prevalence of heart disease, especially heart failure, continues to rise. Among the precipitating aetiologies, ischaemic disease is a leading cause of heart failure. In the context of ischaemia, the myocardium is deprived of oxygen and nutrients, which elicits a cascade of events that provokes cell death. This ischaemic insult is typically coupled with reperfusion, either spontaneous or therapeutically imposed, wherein blood supply is restored to the previously ischaemic tissue. While this intervention limits ischaemic injury, it triggers a new cascade of events that is also harmful, viz. reperfusion injury. In recent years, novel insights have emerged regarding mechanisms of ischaemia-reperfusion injury, and some hold promise as targets of therapeutic relevance. Here, we review a select number of these pathways, focusing on recent discoveries and highlighting prospects for therapeutic manipulation for clinical benefit.
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U2 - 10.1113/JP270953
DO - 10.1113/JP270953
M3 - Review article
C2 - 26173176
AN - SCOPUS:84940567895
SN - 0022-3751
VL - 593
SP - 3773
EP - 3788
JO - Journal of Physiology
JF - Journal of Physiology
IS - 17
ER -