Rohrbach Susanne, Troidl Christian, Hamm Christian, Schulz Rainer
Institute of Physiology, Justus Liebig University Giessen, Giessen, Germany.
IUBMB Life. 2015 Feb;67(2):110-9. doi: 10.1002/iub.1352. Epub 2015 Apr 8.
Occlusion of a coronary artery if maintained for longer period of time results in damage of the cardiac tissue. However, restoration of blood flow to previously ischemic tissue can itself induce further cardiac damage, a phenomenon known as myocardial reperfusion injury. Cardiac homoeostasis is supported by a network of direct and indirect interactions between cardiomyocytes and resident cell types such as fibroblasts, adipocytes, and endothelial cells or invading blood cells. This review will discuss the role of the cellular interplay in ischemia-reperfusion injury from a cardiomyocyte-centered view, although we are aware that other cellular interactions are equally important. We will try to work out currently unresolved questions and potential future directions in the field.
冠状动脉阻塞若持续较长时间会导致心脏组织受损。然而，恢复先前缺血组织的血流本身可引发进一步的心脏损伤，这一现象被称为心肌再灌注损伤。心肌细胞与诸如成纤维细胞、脂肪细胞、内皮细胞等驻留细胞类型或侵入的血细胞之间通过直接和间接相互作用网络维持心脏内环境稳定。本综述将从以心肌细胞为中心的视角探讨细胞间相互作用在缺血再灌注损伤中的作用，尽管我们知道其他细胞间相互作用同样重要。我们将尝试梳理该领域目前尚未解决的问题以及潜在的未来研究方向。
