Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC
Nonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases. The phenotypic umbrella of NAFLD spans from simple and reversible steatosis to nonalcoholic steatohepatitis (NASH), which may worsen into cirrhosis and hepatocellular carcinoma (HCC)....
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MDPI AG
2021-10-01
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| Series: | Biomedicines |
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| Online Access: | https://www.mdpi.com/2227-9059/9/11/1524 |
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| author | Paola Dongiovanni Marica Meroni Miriam Longo Silvia Fargion Anna Ludovica Fracanzani |
| author_facet | Paola Dongiovanni Marica Meroni Miriam Longo Silvia Fargion Anna Ludovica Fracanzani |
| author_sort | Paola Dongiovanni |
| collection | DOAJ |
| description | Nonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases. The phenotypic umbrella of NAFLD spans from simple and reversible steatosis to nonalcoholic steatohepatitis (NASH), which may worsen into cirrhosis and hepatocellular carcinoma (HCC). Notwithstanding, HCC may develop also in the absence of advanced fibrosis, causing a delayed time in diagnosis as a consequence of the lack of HCC screening in these patients. The precise event cascade that may precipitate NASH into HCC is intricate and it entails diverse triggers, encompassing exaggerated immune response, endoplasmic reticulum (ER) and oxidative stress, organelle derangement and DNA aberrancies. All these events may be accelerated by both genetic and environmental factors. On one side, common and rare inherited variations that affect hepatic lipid remodeling, immune microenvironment and cell survival may boost the switching from steatohepatitis to liver cancer, on the other, diet-induced dysbiosis as well as nutritional and behavioral habits may furtherly precipitate tumor onset. Therefore, dietary and lifestyle interventions aimed to restore patients’ health contribute to counteract NASH progression towards HCC. Even more, the combination of therapeutic strategies with dietary advice may maximize benefits, with the pursuit to improve liver function and prolong survival. |
| first_indexed | 2024-03-10T05:41:05Z |
| format | Article |
| id | doaj.art-41ee9aeec43048779c58796f6c87422b |
| institution | Directory Open Access Journal |
| issn | 2227-9059 |
| language | English |
| last_indexed | 2024-03-10T05:41:05Z |
| publishDate | 2021-10-01 |
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| spelling | doaj.art-41ee9aeec43048779c58796f6c87422b2023-11-22T22:29:30ZengMDPI AGBiomedicines2227-90592021-10-01911152410.3390/biomedicines9111524Genetics, Immunity and Nutrition Boost the Switching from NASH to HCCPaola Dongiovanni0Marica Meroni1Miriam Longo2Silvia Fargion3Anna Ludovica Fracanzani4General Medicine and Metabolic Diseases, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Pad. Granelli, 20122 Milan, ItalyGeneral Medicine and Metabolic Diseases, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Pad. Granelli, 20122 Milan, ItalyGeneral Medicine and Metabolic Diseases, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Pad. Granelli, 20122 Milan, ItalyGeneral Medicine and Metabolic Diseases, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Pad. Granelli, 20122 Milan, ItalyGeneral Medicine and Metabolic Diseases, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Pad. Granelli, 20122 Milan, ItalyNonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases. The phenotypic umbrella of NAFLD spans from simple and reversible steatosis to nonalcoholic steatohepatitis (NASH), which may worsen into cirrhosis and hepatocellular carcinoma (HCC). Notwithstanding, HCC may develop also in the absence of advanced fibrosis, causing a delayed time in diagnosis as a consequence of the lack of HCC screening in these patients. The precise event cascade that may precipitate NASH into HCC is intricate and it entails diverse triggers, encompassing exaggerated immune response, endoplasmic reticulum (ER) and oxidative stress, organelle derangement and DNA aberrancies. All these events may be accelerated by both genetic and environmental factors. On one side, common and rare inherited variations that affect hepatic lipid remodeling, immune microenvironment and cell survival may boost the switching from steatohepatitis to liver cancer, on the other, diet-induced dysbiosis as well as nutritional and behavioral habits may furtherly precipitate tumor onset. Therefore, dietary and lifestyle interventions aimed to restore patients’ health contribute to counteract NASH progression towards HCC. Even more, the combination of therapeutic strategies with dietary advice may maximize benefits, with the pursuit to improve liver function and prolong survival.https://www.mdpi.com/2227-9059/9/11/1524NAFLDNASHheritabilityHCCnutrition |
| spellingShingle | Paola Dongiovanni Marica Meroni Miriam Longo Silvia Fargion Anna Ludovica Fracanzani Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC Biomedicines NAFLD NASH heritability HCC nutrition |
| title | Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC |
| title_full | Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC |
| title_fullStr | Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC |
| title_full_unstemmed | Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC |
| title_short | Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC |
| title_sort | genetics immunity and nutrition boost the switching from nash to hcc |
| topic | NAFLD NASH heritability HCC nutrition |
| url | https://www.mdpi.com/2227-9059/9/11/1524 |
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