Department of Clinical and Experimental Medicine, Policlinic "G. Martino", University of Messina, 98100 Messina, Italy.
Section of Pharmacology, Department of Clinical and Experimental Medicine, University of Messina, 98100 Messina, Italy.
Med Sci (Basel). 2021 Mar 1;9(1):16. doi: 10.3390/medsci9010016.
The ischemic injury caused by myocardial infarction activates a complex healing process wherein a powerful inflammatory response and a reparative phase follow and balance each other. An intricate network of mediators finely orchestrate a large variety of cellular subtypes throughout molecular signaling pathways that determine the intensity and duration of each phase. At the end of this process, the necrotic tissue is replaced with a fibrotic scar whose quality strictly depends on the delicate balance resulting from the interaction between multiple actors involved in fibrogenesis. An inflammatory or reparative dysregulation, both in term of excess and deficiency, may cause ventricular dysfunction and life-threatening arrhythmias that heavily affect clinical outcome. This review discusses cellular process and molecular signaling pathways that determine fibrosis and the imaging technique that can characterize the clinical impact of this process in-vivo.
心肌梗死引起的缺血性损伤激活了一个复杂的修复过程，其中强烈的炎症反应和修复阶段相互跟随并平衡。在分子信号通路中，有一个错综复杂的介质网络精细地协调着大量不同的细胞亚型，这些信号通路决定了每个阶段的强度和持续时间。在这个过程结束时，坏死组织被纤维化疤痕所取代，其质量严格取决于纤维化过程中涉及的多个因素之间相互作用产生的微妙平衡。炎症或修复的失调，无论是过度还是不足，都可能导致心室功能障碍和危及生命的心律失常，严重影响临床结果。这篇综述讨论了决定纤维化的细胞过程和分子信号通路，以及可以在体内描述这一过程临床影响的成像技术。
