Assessment of Genetic Aspects of Non-alcoholic Fatty Liver and Premature Cardiovascular Events.
Cardiovascular disease
Gene polymorphism
Genetic aspect
Non-alcoholic fatty liver disease
Journal
Middle East journal of digestive diseases
ISSN: 2008-5230
Titre abrégé: Middle East J Dig Dis
Pays: Iran
ID NLM: 101535395
Informations de publication
Date de publication:
Apr 2020
Apr 2020
Historique:
entrez:
7
7
2020
pubmed:
7
7
2020
medline:
7
7
2020
Statut:
ppublish
Résumé
Recent evidence has demonstrated a strong interplay and multifaceted relationship between non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). CVD is the major cause of death in patients with NAFLD. NAFLD also has strong associations with diabetes and metabolic syndrome. In this comprehensive review, we aimed to overview the primary environmental and genetic risk factors of NAFLD, and CVD and also focus on the genetic aspects of these two disorders. NAFLD and CVD are both heterogeneous diseases with common genetic and molecular pathways. We have searched for the latest published articles regarding this matter and tried to provide an overview of recent insights into the genetic aspects of NAFLD and CVD. The common genetic and molecular pathways involved in NAFLD and CVD are insulin resistance (IR), subclinical inflammation, oxidative stress, and atherogenic dyslipidemia. According to an investigation, the exact associations between genomic characteristics of NAFLD and CVD and casual relationships are not fully determined. Different gene polymorphisms have been identified as the genetic components of the NAFLDCVD association. Some of the most documented ones of these gene polymorphisms are patatin-like phospholipase domain-containing protein 3 (PNPLA3), transmembrane 6 superfamily member 2 (TM6SF2), hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13), adiponectin-encoding gene (ADIPOQ), apolipoprotein C3 (APOC3), peroxisome proliferator-activated receptors (PPAR), leptin receptor (LEPR), sterol regulatory element-binding proteins (SREBP), tumor necrosis factor-alpha (TNF-α), microsomal triglyceride transfer protein (MTTP), manganese superoxide dismutase (MnSOD), membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), and mutation in DYRK1B that substitutes cysteine for arginine at position 102 in kinase-like domain. Further cohort studies with a significant sample size using advanced genomic assessments and next-generation sequencing techniques are needed to shed more light on genetic associations between NAFLD and CVD.
Identifiants
pubmed: 32626560
doi: 10.34172/mejdd.2020.166
pmc: PMC7320986
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
65-88Informations de copyright
© 2020 The Author(s).
Déclaration de conflit d'intérêts
CONFLICT OF INTEREST The authors declare no conflict of interest related to this work.
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