Ask about this productRelated genes to: LENG4 antibody
- Gene:
- MBOAT7 NIH gene
- Name:
- membrane bound O-acyltransferase domain containing 7
- Previous symbol:
- LENG4
- Synonyms:
- BB1, hMBOA-7, LPLAT
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2018-03-06
Related products to: LENG4 antibody
Related articles to: LENG4 antibody
- Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease worldwide. Although genetic variants are linked to MASLD progression, whether their associations with fibrosis severity are consistent across clinical contexts remains unclear. - Source: PubMed
Lee Mei-HsuanStepanova MariaEstep MichaelYou Yan-LingLiu Xia-Rongde Avila LeylaLam BrianYu Ming-LungYounossi Zobair M - Early prevention of dyslipidemia is critical for reducing the future onset of atherosclerosis and atherosclerotic cardiovascular diseases. Although lifestyle interventions have been recommended, the interactions between common genetic variants and modifiable habits in young populations remain unclear. Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7) has been implicated in lipid metabolism and steatotic liver disease; however, its role in early atherosclerosis is poorly understood. Associations between the MBOAT7 rs641738 genotype, lifestyle habits, and atherogenic lipid profiles were assessed in young adults and adolescents. - Source: PubMed
Publication date: 2026/05/06
Kado AkiraInoue YukikoTsutsumi TakeyaFujishiro MitsuhiroYanagimoto Shintaro - The long-term impact of HCV cure on hepatic and metabolic outcomes in patients with type 2 diabetes (T2D) remains insufficiently defined. This study evaluated T2D-related vascular complications, liver disease progression and overall survival over 9 years of follow-up, also exploring genetic variability contribution. - Source: PubMed
Asero CleliaFranzè Maria StellaMaltese TeresaLa Spada AlbertoLombardo DanieleGrisanti ClaudiaRusso GiuseppinaGiandalia AnnalisaPitrone ConcettaFilomia RobertoCaccamo GaiaSaitta CarloLicata AnnaPollicino TeresaCacciola Irene - Metabolic dysfunction-associated fatty liver disease (MAFLD), recently redefined from non-alcoholic fatty liver disease (NAFLD), highlights the central role of metabolic dysfunction in its pathophysiology. The L-α-lysophosphatidylinositol/G protein-coupled receptor 55 (LPI/GPR55) axis, an element of the endocannabinoidome, has emerged as a key driver behind liver disease progression, leading to the progression of metabolic dysfunction associated steatohepatitis (MASH). Implicated in hepatic lipid accumulation, inflammation and fibrosis, this axis has detrimental effects in hepatocytes, Kupffer cells and hepatic stellate cells. Furthermore, recent evidence suggests that this axis induces de novo lipogenesis, promoting pro-inflammatory cytokine production, leading to fibrosis and the transition toward a steatotic liver. The enzyme membrane-bound O-acyltransferase domain-containing 7 (MBOAT7) modulates this axis by acylation of LPI, exacerbating hepatic steatosis and insulin resistance. Until recently, no pharmacologic treatments were approved for MAFLD. However, resmetirom received FDA approval in March 2024 for the treatment of MASH, and semaglutide (Wegovy) was granted accelerated FDA approval in August 2025 for MASH with moderate-to-advanced fibrosis. Additional agents such as tirzepatide and retatrutide remain in late-stage clinical development. We propose that targeting the endocannabinoidome, specifically the LPI/GPR55 axis, represents a promising therapeutic strategy for liver disease. Previous attempts to target GPR55 therapeutically have involved small-molecule agonists and phytocannabinoids with antagonistic activity. However, progress remains limited due to the context-specific roles of GPR55 across different tissues and signalling pathways. As such, future strategies involving the LPI/GPR55 axis must focus on hepatic-specific GPR55 modulation using selective ligands and advanced delivery systems, mitigating off-target effects. This review elucidates the mechanistic role of the LPI/GPR55 axis, combining the role of MBOAT7 in the pathophysiology of metabolic-associated liver disease. - Source: PubMed
Lian JeromeLareu Ricky RPatil MohanFalasca Marco - Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as NAFLD (non-alcoholic fatty liver disease), is a growing global concern, affecting nearly a third of the world’s population. This umbrella term covers a range of liver pathologies, from reversible disease stages like simple steatosis, to irreversible conditions such as cirrhosis and hepatocellular carcinoma (HCC). MASLD, which may result from metabolic risk factors like obesity and type 2 diabetes, is projected to increase due to a rise in sedentary lifestyles. This review addresses genetic influences that predispose to disease development, including the role of risk-conferring and protective/preventive alleles. The epistatic relationships between genetic variants can significantly influence the development and progression of MASLD. Key genetic variants, such as those located in the , , and genes, often interact to exacerbate MASLD severity and play key roles in lipid metabolism and liver inflammation. For example, the co-expression of certain and variants increases the risk of advanced fibrosis and HCC. Some variants located in and offer protective effects, reducing the risk of severe liver disease despite comorbidities such as obesity, and can mitigate the harmful effects of these risk alleles. Additionally, the potential of polygenic risk scores (PRS) to predict MASLD development and its complications is also discussed, although challenges remain, particularly in underrepresented populations due to the lack of comprehensive catalogues of genetic variation. Understanding these complex gene-gene interactions and the role of the environment underscores the importance of considering epistatic relationships when assessing MASLD risk and developing personalized therapeutic strategies, which could ease the future burden on healthcare systems. - Source: PubMed
Publication date: 2026/03/02
Arriaga-González Fernanda Gde Jesús Castañeda-Córdova FelipeDíaz-Muñoz MauricioHoare MatthewAdams David JRobles-Espinoza Carla DanielaMolina-Aguilar Christian