Laboratory of Atherosclerosis and Vascular Biology, State University of Campinas, Campinas, Brazil.
Laboratory of Atherosclerosis and Vascular Biology, State University of Campinas, Campinas, Brazil.
Adv Clin Chem. 2018;84:39-79. doi: 10.1016/bs.acc.2017.12.002. Epub 2018 Feb 2.
The occlusion of a coronary artery by a thrombus generated on a ruptured atherosclerotic plaque has been pursued in the last decades as a determining event for the clinical outcome after myocardial infarction (MI). Yet, MI causes a cell death wave front, which triggers an inflammatory response to clear cellular debris, and which in excess can double the myocardial lesion and influence the clinical prognosis in the short and long term. Accordingly, proper, timely regulated inflammatory response has now been considered a second pivotal player in cardiac recovery after MI justifying the search for pharmacological strategies to modulate inflammatory effectors. This chapter reviews the key events and the main effectors of inflammation after myocardial ischemic insult, as well as the contribution of this phenomenon to the progression of atherosclerosis.
在过去几十年中,人们一直关注冠状动脉被破裂的动脉粥样硬化斑块上形成的血栓阻塞,这是心肌梗死 (MI) 后临床转归的决定性事件。然而,MI 会引发细胞死亡波前,从而引发炎症反应以清除细胞碎片,过度的炎症反应会使心肌损伤加倍,并在短期和长期内影响临床预后。因此,适当、及时的调节炎症反应现在被认为是 MI 后心脏恢复的第二个关键因素,这也证明了寻找调节炎症效应器的药理学策略是合理的。本章回顾了心肌缺血损伤后炎症的关键事件和主要效应器,以及这一现象对动脉粥样硬化进展的贡献。