Personalized medicine in nonalcoholic fatty liver disease

Genetics in non-alcoholic fatty liver disease: The role of risk alleles through the lens of immune response

“…Likewise, while translating GWAS / EWAS / and PHEWAS signals into clinical applications has been slow, genetic knowledge in NAFLD and NASH may significantly improve disease management and monitoring. The accumulated genetic knowledge is now being used to predict disease outcomes and personalized medicine in the field of NAFLD 8,51,52 and for repurposing drugs and or select potential actionable targets to treat the disease 4,53,54 This figure provides a functional enrichment analysis of the genes and proteins associated with NAFLD and the immune system, the information of which has been extracted from heterogeneous genomic and proteomic resources using the FunRich program (55,56).…”

“…Likewise, while translating GWAS, EWAS, and PHEWAS signals into clinical applications has been slow, genetic knowledge in NAFLD and NASH may significantly improve disease management and monitoring. The accumulated genetic knowledge is now being used to predict disease outcomes and personalized medicine in the field of NAFLD [ 8 , 51 , 52 ], and to repurpose drugs and/or select potential actionable targets to treat the disease [ 4 , 53 , 54 ].…”

“…Knowledge of the genetic component of non-alcoholic fatty liver disease (NAFLD) has grown exponentially over the last 10-15 years [3][4][5][6][7] . With this knowledge it becomes possible to translate information of risk alleles and its effects on the disease biology into clinical applications 6,8 . Most importantly, knowledge on the genetic component of NAFLD may be leveraged to identify individuals at risk and/or to estimate the risk of severe histological outcomes, including NASH (non-alcoholic steatohepatitis)-fibrosis, cirrhosis, and hepatocellular carcinoma 6,8 .…”

The effects of moderate alcohol consumption on non-alcoholic fatty liver disease

“…Also, single nucleotide polymorphisms in patatin-like phospholipase domain-containing 3, transmembrane 6 superfamily member 2, membrane bound O-acyltransferase domain containing 7, 17-β hydroxysteroid dehydrogenase 13 gene are significant genetic risk factors for NAFLD and ARLD. [11][12][13][14][15] These two entities are difficult to distinguish as both histologically include a certain degree of steatosis, lobular inflammation, and ballooning. 16 However, these two conditions are distinguished by excessive alcohol consumption based on history taking and questionnaire, and the amount of safe alcohol consumption accepted as "non-alcoholic" is disputed.…”

Correspondence on Editorial regarding “Identification of signature gene set as highly accurate determination of MASLD progression”

“…We express our deep gratitude to Dr. Pirola and Dr. Sookoian for their interest in our research [ 1 , 2 ]. The severity of metabolic-associated steatohepatitis liver disease (MASLD), which is characterized by the accumulation of fat in the liver, inflammation, and liver cell damage, is significant.…”