New Insights Into the Role of Autophagy in Liver Surgery in the Setting of Metabolic Syndrome and Related Diseases.
New Insights Into the Role of Autophagy in Liver Surgery in the Setting of Metabolic Syndrome and Related Diseases.
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DOI：
10.3389/fcell.2021.670273
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发表时间：
2021
影响因子：
5.5
通讯作者：
Casillas-Ramírez A
中科院分区：
文献类型：
--
作者：
Álvarez-Mercado AI;Rojano-Alfonso C;Micó-Carnero M;Caballeria-Casals A;Peralta C;Casillas-Ramírez A
内脏性肥胖是代谢综合征的一个重要组成部分，代谢综合征是包括糖尿病和胰岛素抵抗在内的一系列疾病。这些代谢紊乱的组合损害肝功能，表现为非酒精性脂肪性肝病（NAFLD）。NAFLD是肝功能异常的常见原因，大量研究已经证实肝脂肪变性在肝切除和移植不可避免地发生的缺血-再灌注（I/R）损伤中的巨大有害作用。因此，脂肪变性肝在肝切除术后出现术后并发症的频率更高，并且使用NAFLD供体的肝移植与受体术后发病率和死亡率的风险增加有关。糖尿病是另一种与met相关的代谢紊乱，也会加重肝脏I/R损伤，与NAFLD相似，糖尿病与肝脏手术后预后不良相关。由于met、NAFLD和糖尿病患病率的大幅增加，它们的关联在人群中很常见，因此在需要肝切除术的患者和潜在的肝移植供者中也很常见。这种情况需要改进治疗方法，以改善患有代谢性疾病和接受肝脏手术的患者的术后效果；从这个意义上说，设计治疗策略的基础是深入了解met相关疾病和I/R损伤对肝组织影响的分子信号通路。所有这些疾病的共同点是自噬。事实上，在肥胖的情况下，肝细胞的自噬大大减少，并改变肝脏的线粒体功能。在胰岛素抵抗的情况下，肝脏的自噬受到抑制，这与脂质积累有关，这是NAFLD的一个危险因素。此外，肝I/R损伤中发生的氧化应激促进自噬。本综述旨在揭示自噬在肝脏手术和代谢性疾病中的作用，这可能会导致发现有效的治疗靶点，可以从实验室转化为临床实践，以改善存在一种或多种代谢性疾病的肝脏手术的术后效果。
Visceral obesity is an important component of metabolic syndrome, a cluster of diseases that also includes diabetes and insulin resistance. A combination of these metabolic disorders damages liver function, which manifests as non-alcoholic fatty liver disease (NAFLD). NAFLD is a common cause of abnormal liver function, and numerous studies have established the enormously deleterious role of hepatic steatosis in ischemia-reperfusion (I/R) injury that inevitably occurs in both liver resection and transplantation. Thus, steatotic livers exhibit a higher frequency of post-surgical complications after hepatectomy, and using liver grafts from donors with NAFLD is associated with an increased risk of post-surgical morbidity and mortality in the recipient. Diabetes, another MetS-related metabolic disorder, also worsens hepatic I/R injury, and similar to NAFLD, diabetes is associated with a poor prognosis after liver surgery. Due to the large increase in the prevalence of MetS, NAFLD, and diabetes, their association is frequent in the population and therefore, in patients requiring liver resection and in potential liver graft donors. This scenario requires advancement in therapies to improve postoperative results in patients suffering from metabolic diseases and undergoing liver surgery; and in this sense, the bases for designing therapeutic strategies are in-depth knowledge about the molecular signaling pathways underlying the effects of MetS-related diseases and I/R injury on liver tissue. A common denominator in all these diseases is autophagy. In fact, in the context of obesity, autophagy is profoundly diminished in hepatocytes and alters mitochondrial functions in the liver. In insulin resistance conditions, there is a suppression of autophagy in the liver, which is associated with the accumulation of lipids, being this is a risk factor for NAFLD. Also, oxidative stress occurring in hepatic I/R injury promotes autophagy. The present review aims to shed some light on the role of autophagy in livers undergoing surgery and also suffering from metabolic diseases, which may lead to the discovery of effective therapeutic targets that could be translated from laboratory to clinical practice, to improve postoperative results of liver surgeries when performed in the presence of one or more metabolic diseases.
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