title: Insulin-Like Growth Factor-1 Deficiency and Cirrhosis Establishment.
abstract: 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.
authors.affiliation: Centro de Investigacion Transferencia en Salud (CITES), Escuela Nacional de Medicina, Tecnologico de Monterrey, and Institute of Liver Diseases, Hospital San Jose, Tecnologico de Monterrey, Monterrey, Nuevo Leon, Mexico.
authors.forename: Rocio G
authors.initials: RG
authors.lastname: de la Garza
authors.affiliation: Centro de Investigacion Transferencia en Salud (CITES), Escuela Nacional de Medicina, Tecnologico de Monterrey, and Institute of Liver Diseases, Hospital San Jose, Tecnologico de Monterrey, Monterrey, Nuevo Leon, Mexico.
authors.forename: Luis Alonso
authors.initials: LA
authors.lastname: Morales-Garza
authors.affiliation: Centro de Investigacion Transferencia en Salud (CITES), Escuela Nacional de Medicina, Tecnologico de Monterrey, and Institute of Liver Diseases, Hospital San Jose, Tecnologico de Monterrey, Monterrey, Nuevo Leon, Mexico.
authors.forename: Irene
authors.initials: I
authors.lastname: Martin-Estal
authors.affiliation: Centro de Investigacion Transferencia en Salud (CITES), Escuela Nacional de Medicina, Tecnologico de Monterrey, and Institute of Liver Diseases, Hospital San Jose, Tecnologico de Monterrey, Monterrey, Nuevo Leon, Mexico; Fundacion de Investigacion HM Hospitales, Madrid, Spain.
authors.forename: Inma
authors.initials: I
authors.lastname: Castilla-Cortazar
keywords: Acute liver damage; Fibrogenesis; GH/IGF-1 axis; IGF-1; Mitochondrial protection; Non-alcoholic fatty liver disease; Oxidative damage; Steatosis