McCormick James, Knight Richard A, Barry Sean P, Scarabelli Tiziano M, Abounit Kadija, Latchman David S, Stephanou Anastasis
The Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH.
Front Biosci (Elite Ed). 2012 Jan 1;4(6):2131-41. doi: 10.2741/e530.
Cardiovascular disease is a leading cause of death worldwide, particularly in Western societies. During an ischaemic insult, ventricular pressure from the heart is diminished as a result of cardiac myocyte death by necrosis and apoptosis. Autophagy is a process whereby cells catabolise intracellular proteins in order to generate ATP in times of stress such as nutrient starvation and hypoxia. Emerging evidence suggests that autophagy plays a positive role in cardiac myocyte survival during periods of cellular stress performing an important damage limitation function. By promoting cell survival, cardiac myocyte loss is reduced thereby minimising the potential of heart failure. In contrast, it has been reported that autophagy can also be a form of cell death. By considering the various animal models of autophagy, we examine the role of the Signal Transducers and Activator of Transcription (STAT) proteins in the autophagic response. Additionally we review the role of the tumour suppressor, p53 and its family member p73 and their potential role in the autophagic response.
心血管疾病是全球主要的死亡原因，在西方社会尤为如此。在缺血性损伤期间，由于心肌细胞因坏死和凋亡而死亡，心脏的心室压力会降低。自噬是细胞在营养饥饿和缺氧等应激状态下分解细胞内蛋白质以产生ATP的过程。新出现的证据表明，自噬在细胞应激期间的心肌细胞存活中发挥着积极作用，具有重要的损伤限制功能。通过促进细胞存活，减少心肌细胞损失，从而将心力衰竭的可能性降至最低。相比之下，据报道自噬也可能是一种细胞死亡形式。通过研究各种自噬动物模型，我们探讨了信号转导子和转录激活子（STAT）蛋白在自噬反应中的作用。此外，我们还综述了肿瘤抑制因子p53及其家族成员p73的作用以及它们在自噬反应中的潜在作用。
