期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 21, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms21010040
关键词
Metabolic syndrome; NAFLD; NASH; cirrhosis; HCC; sphingolipids; ceramide; S1P; sphingomyelin; metabolomics; lipidomics
资金
- Ministerio de Economia, Industria y Competitividad [SAF2017-87301-R]
- Gobierno Vasco-Departamento de Salud [2013111114]
- BIOEF (Basque Foundation for Innovation and Health Research: EiTB Maratoia) [BIO15/CA/016/BD]
- ELKARTEK 2016, Departamento de Industria del Gobierno Vasco
- Asociacion Espanola contra el Cancer
- Daniel Alagille award from EASL
- Fundacion Cientifica de la Asociacion Espanola Contra el Cancer (AECC Scientific Foundation) Rare Tumor Calls 2017
- La Caixa Foundation Program
- Gobierno Vasco-Departamento de Educacion
- MINECO [SEV-2016-0644]
Non-alcoholic fatty liver disease (NAFLD) has emerged as one of the main causes of chronic liver disease worldwide. NAFLD comprises a group of conditions characterized by the accumulation of hepatic lipids that can eventually lead to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), the fifth most common cancer type with a poor survival rate. In this context, several works have pointed out perturbations in lipid metabolism and, particularly, changes in bioactive sphingolipids, as a hallmark of NAFLD and derived HCC. In the present work, we have reviewed existing literature about sphingolipids and the development of NAFLD and NAFLD-derived HCC. During metabolic syndrome, considered a risk factor for steatosis development, an increase in ceramide and sphigosine-1-phosphate (S1P) have been reported. Likewise, other reports have highlighted that increased sphingomyelin and ceramide content is observed during steatosis and NASH. Ceramide also plays a role in liver fibrosis and cirrhosis, acting synergistically with S1P. Finally, during HCC, metabolic fluxes are redirected to reduce cellular ceramide levels whilst increasing S1P to support tumor growth.
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