Departments of Surgery, University of Texas Southwestern Medical Center, 75390 Dallas, TX, USA.
Department of Developmental Cell Biology, School of Life Sciences, China Medical University, 77 Puhe Road, Shenbei New District, 110122 Shenyang, China.
Cells. 2019 Feb 10;8(2):141. doi: 10.3390/cells8020141.
Sepsis is a leading cause of death in intensive care units, and cardiac dysfunction is an identified serious component of the multi-organ failure associated with this critical condition. This review summarized the current discoveries and hypothesizes of how autophagy changes in the heart during sepsis and the underlying mechanisms. Recent investigations suggest that specific activation of autophagy initiation factor Beclin-1 has a potential to protect cardiac mitochondria, attenuate inflammation, and improve cardiac function in sepsis. Accordingly, pharmacological interventions targeting this pathway have a potential to become an effective approach to control sepsis outcomes. The role of autophagy during sepsis pathogenesis has been under intensive investigation in recent years. It is expected that developing therapeutic approaches with specificities targeting at autophagy regulatory factors may provide new opportunities to alleviate organ dysfunction caused by maladaptive autophagy during sepsis.
脓毒症是重症监护病房死亡的主要原因,而心脏功能障碍是与这种危急情况相关的多器官衰竭的一个严重组成部分。这篇综述总结了目前关于脓毒症期间自噬在心脏中变化的发现和假说,以及潜在的机制。最近的研究表明,特定地激活自噬起始因子 Beclin-1 有可能保护心脏线粒体、减轻炎症,并改善脓毒症中的心脏功能。因此,针对该途径的药理学干预有可能成为控制脓毒症结果的有效方法。近年来,自噬在脓毒症发病机制中的作用受到了广泛的研究。预计开发具有针对自噬调节因子特异性的治疗方法可能为缓解脓毒症期间适应性自噬引起的器官功能障碍提供新的机会。