安普克
限制
再灌注损伤
缺血
医学
疾病
心肌缺血
缺血性损伤
神经科学
生物信息学
心脏病学
药理学
内科学
生物
蛋白激酶A
细胞生物学
磷酸化
工程类
机械工程
标识
DOI:10.1016/j.bcp.2011.04.004
摘要
Ischemic heart disease stands as the number one leading cause of death in the United States. Current interventions rely on the immediate restoration of blood flow to the ischemic area; however, this in turn may trigger a series of undesirable events that are further injurious to the myocardium, termed ischemia/reperfusion (I/R) injury. Therefore, there is a need for novel therapeutic strategies aimed at limiting the extent of myocardial injury. Yet, the molecular mechanisms responsible for I/R injury remain largely indefinable. Research efforts are currently investigating various signaling mechanisms to be used for potential targets limiting cardiac injury due to such cardiovascular events. In this review, we highlight two potential molecular targets, PPAR-γ and AMPK, which have been extensively reported to have various cardioprotective capabilities against I/R injury. Although functionally different, the pathways these proteins mediate seem to intersect and possibly act synergistically potentiating a cardioprotective response.
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