Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease
Nonalcoholic fatty liver disease (NAFLD), the most prominent cause of chronic liver disease worldwide, is a rapidly growing epidemic. It consists of a wide range of liver diseases, from steatosis to nonalcoholic steatohepatitis, and predisposes patients to liver fibrosis, cirrhosis, and even hepatoc...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-08-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/16/12864 |
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| author | Ioanna Aggeletopoulou Maria Kalafateli Efthymios P. Tsounis Christos Triantos |
| author_facet | Ioanna Aggeletopoulou Maria Kalafateli Efthymios P. Tsounis Christos Triantos |
| author_sort | Ioanna Aggeletopoulou |
| collection | DOAJ |
| description | Nonalcoholic fatty liver disease (NAFLD), the most prominent cause of chronic liver disease worldwide, is a rapidly growing epidemic. It consists of a wide range of liver diseases, from steatosis to nonalcoholic steatohepatitis, and predisposes patients to liver fibrosis, cirrhosis, and even hepatocellular carcinoma. NAFLD is strongly correlated with obesity; however, it has been extensively reported among lean/nonobese individuals in recent years. Although lean patients demonstrate a lower prevalence of diabetes mellitus, central obesity, dyslipidemia, hypertension, and metabolic syndrome, a percentage of these patients may develop steatohepatitis, advanced liver fibrosis, and cardiovascular disease, and have increased all-cause mortality. The pathophysiological mechanisms of lean NAFLD remain vague. Studies have reported that lean NAFLD demonstrates a close association with environmental factors, genetic predisposition, and epigenetic modifications. In this review, we aim to discuss and summarize the epigenetic mechanisms involved in lean NAFLD and to introduce the interaction between epigenetic patterns and genetic or non genetic factors. Several epigenetic mechanisms have been implicated in the regulation of lean NAFLD. These include DNA methylation, histone modifications, and noncoding-RNA-mediated gene regulation. Epigenetics is an area of special interest in the setting of lean NAFLD as it could provide new insights into the therapeutic options and noninvasive biomarkers that target this under-recognized and challenging disorder. |
| first_indexed | 2024-03-10T23:52:40Z |
| format | Article |
| id | doaj.art-bc5243db9833418d934e4624fa9728a8 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T23:52:40Z |
| publishDate | 2023-08-01 |
| publisher | MDPI AG |
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| series | International Journal of Molecular Sciences |
| spelling | doaj.art-bc5243db9833418d934e4624fa9728a82023-11-19T01:31:02ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-08-0124161286410.3390/ijms241612864Epigenetic Regulation in Lean Nonalcoholic Fatty Liver DiseaseIoanna Aggeletopoulou0Maria Kalafateli1Efthymios P. Tsounis2Christos Triantos3Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, 26504 Patras, GreeceDepartment of Gastroenterology, General Hospital of Patras, 26332 Patras, GreeceDivision of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, 26504 Patras, GreeceDivision of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, 26504 Patras, GreeceNonalcoholic fatty liver disease (NAFLD), the most prominent cause of chronic liver disease worldwide, is a rapidly growing epidemic. It consists of a wide range of liver diseases, from steatosis to nonalcoholic steatohepatitis, and predisposes patients to liver fibrosis, cirrhosis, and even hepatocellular carcinoma. NAFLD is strongly correlated with obesity; however, it has been extensively reported among lean/nonobese individuals in recent years. Although lean patients demonstrate a lower prevalence of diabetes mellitus, central obesity, dyslipidemia, hypertension, and metabolic syndrome, a percentage of these patients may develop steatohepatitis, advanced liver fibrosis, and cardiovascular disease, and have increased all-cause mortality. The pathophysiological mechanisms of lean NAFLD remain vague. Studies have reported that lean NAFLD demonstrates a close association with environmental factors, genetic predisposition, and epigenetic modifications. In this review, we aim to discuss and summarize the epigenetic mechanisms involved in lean NAFLD and to introduce the interaction between epigenetic patterns and genetic or non genetic factors. Several epigenetic mechanisms have been implicated in the regulation of lean NAFLD. These include DNA methylation, histone modifications, and noncoding-RNA-mediated gene regulation. Epigenetics is an area of special interest in the setting of lean NAFLD as it could provide new insights into the therapeutic options and noninvasive biomarkers that target this under-recognized and challenging disorder.https://www.mdpi.com/1422-0067/24/16/12864epigeneticsnonalcoholic fatty liver diseaselean NAFLDnonobese NAFLDepigenetic regulationDNA methylation |
| spellingShingle | Ioanna Aggeletopoulou Maria Kalafateli Efthymios P. Tsounis Christos Triantos Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease International Journal of Molecular Sciences epigenetics nonalcoholic fatty liver disease lean NAFLD nonobese NAFLD epigenetic regulation DNA methylation |
| title | Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease |
| title_full | Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease |
| title_fullStr | Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease |
| title_full_unstemmed | Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease |
| title_short | Epigenetic Regulation in Lean Nonalcoholic Fatty Liver Disease |
| title_sort | epigenetic regulation in lean nonalcoholic fatty liver disease |
| topic | epigenetics nonalcoholic fatty liver disease lean NAFLD nonobese NAFLD epigenetic regulation DNA methylation |
| url | https://www.mdpi.com/1422-0067/24/16/12864 |
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