Insulin-Like Growth Factor-1 Deficiency and Cirrhosis Establishment.
Insulin-Like Growth Factor-1 Deficiency and Cirrhosis Establishment.
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DOI：
10.14740/jocmr2761w
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发表时间：
2017-04-01
期刊：
影响因子：
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通讯作者：
Castilla-Cortazar, Inma
中科院分区：
文献类型：
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作者：
de la Garza, Rocio G;Morales-Garza, Luis Alonso;Castilla-Cortazar, Inma
肝硬变是慢性肝损伤的最后阶段，可由不同因素引起，如酒精、伴有肝脏脂肪变性的代谢综合征、自身免疫性疾病、药物、毒素和病毒感染等。如今，肝硬变是一个重要的健康问题，它是发病率和死亡率不断增加的原因，是全球第14大最常见的死亡原因。导致纤维化并最终导致肝硬变的生理病理途径部分取决于病因。然而，在这个复杂的机制中，有一些共同的特征。最近，研究表明，肝硬变是一个动态的过程，可以通过改变来延缓或逆转纤维化。此外，当肝硬变已经建立时，胰岛素样生长因子-1(IGF-1)缺乏或可获得性降低是一种常见的情况，与导致肝硬变的慢性肝损伤的病因无关。IGF-1的缺乏严重促进了肝硬变患者的进行性营养不良，增加了肝脏建立炎性和氧化微环境并伴有线粒体功能障碍的脆弱性。在这种情况下，肝硬变患者的IGF-1缺乏可以证明这些个体的一些共同特征是合理的。已经在动物和人类身上进行了几项研究，以测试IGF-1的替代作为一种可能的治疗选择，结果令人振奋。
Cirrhosis represents the final stage of chronic liver damage, which can be due to different factors such as alcohol, metabolic syndrome with liver steatosis, autoimmune diseases, drugs, toxins, and viral infection, among others. Nowadays, cirrhosis is an important health problem and it is an increasing cause of morbidity and mortality, being the 14th most common cause of death worldwide. The physiopathological pathways that lead to fibrosis and finally cirrhosis partly depend on the etiology. Nevertheless, some common features are shared in this complex mechanism. Recently, it has been demonstrated that cirrhosis is a dynamic process that can be altered in order to delay or revert fibrosis. In addition, when cirrhosis has been established, insulin-like growth factor-1 (IGF-1) deficiency or reduced availability is a common condition, independently of the etiology of chronic liver damage that leads to cirrhosis. IGF-1 deprivation seriously contributes to the progressive malnutrition of cirrhotic patient, increasing the vulnerability of the liver to establish an inflammatory and oxidative microenvironment with mitochondrial dysfunction. In this context, IGF-1 deficiency in cirrhotic patients can justify some of the common characteristics of these individuals. Several studies in animals and humans have been done in order to test the replacement of IGF-1 as a possible therapeutic option, with promising results.