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 steatohepatitis (MASH) represents a major global health burden, bridging isolated steatosis, progressive fibrosis and hepatocellular carcinoma. Recent paradigms highlight ferroptosis, an iron-dependent, lipid-peroxidation-driven form of regulated cell death, as a primary lytic initiating event in metabolic liver injury. In this review, we delineate the ferroptosis-immune axis in MASH, characterising it as a self-amplifying, bidirectional circuit. In this framework, parenchymal ferroptotic rupture and damage-associated molecular pattern emission drive myeloid activation and pro-inflammatory cytokine release. This inflammatory microenvironment reciprocally triggers cell-autonomous Kupffer cell ferroptosis and homeostatic collapse. We establish a novel cell-type-specific transcriptomic framework governed by a core four-gene signature (, , and ) that maps the transition from early metabolic stress to advanced structural remodelling. Furthermore, we decode the substrate paradox of polyunsaturated fatty acids, illustrating how their role shifts from physiological signalling to executioner substrates when antioxidant systems collapse. This biophysical vulnerability is heavily primed by inherited gene polymorphisms, including , and By evaluating the sexual dimorphism embedded within these pathways, specifically how the DTL-PROX1 axis dictates distinct iron accumulation rates and lipid peroxidation sensitivities, we propose precise clinical stratification strategies. Finally, we outline actionable translational avenues, highlighting how targeting the ferroptosis-immune axis offers a highly specific therapeutic window to arrest lipotoxicity, suppress inflammation and disrupt oncogenic priming before irreversible tissue remodelling occurs. - Source: PubMed
Publication date: 2026/09/10
Kuchay Mohammad ShafiCubero Francisco JavierRamos-Molina Bruno - Genetic variants involved in lipid and glucose metabolism have been implicated in liver disease progression and hepatocellular carcinoma (HCC) development in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). However, their prognostic role in patients with established HCC remains unclear. We aimed to investigate the association between MASLD-related genetic variants and overall survival (OS) in patients with MASLD-related HCC. - Source: PubMed
Publication date: 2026/08/12
Guariglia MartaCaviglia Gian PaoloGaia SilviaRosso ChiaraRolle EmanuelaSaba FrancescaDileo EleonoraSilvestri Gemma MartinaArmandi AngeloCarucci PatriziaBugianesi Elisabetta - Metabolic dysfunction-associated steatotic liver disease (MASLD) has traditionally been conceptualized as a predominantly metabolic disorder driven by obesity and insulin resistance. However, recent advances in human genetics have revealed a more complex picture that encompasses germline susceptibility variants, protective loss-of-function alleles, polygenic risk models, and somatic clonal evolution. Since the discovery of PNPLA3 (patatin-like phospholipase domain-containing 3) I148M, multiple loci-including TM6SF2, MBOAT7, GCKR, HSD17B13, MTARC1, GPAM, and CIDEB-have substantially expanded the mechanistic understanding of disease heterogeneity and hepatocellular vulnerability. Recent studies integrating partitioned polygenic risk scores and unsupervised phenotypic clustering suggest that MASLD may be organized into at least two predominant subtypes: a liver-specific subtype characterized by intrinsic hepatocellular susceptibility, and a cardiometabolic subtype associated with systemic metabolic dysfunction and increased cardiovascular risk. Analyses of cirrhotic liver tissue have, in turn, demonstrated somatic clonal expansion of hepatocytes harboring adaptive metabolic mutations, adding an evolutionary dimension to advanced disease. On this basis, we propose an integrated LS/CM/C framework encompassing liver-specific (LS), cardiometabolic (CM), and clonal (C) components. This model offers a conceptual structure that links germline genetics, metabolic heterogeneity, somatic adaptation, and emerging pharmacogenomic strategies. The recent development of genotype-directed therapies targeting PNPLA3 and HSD17B13, together with the approval of resmetirom and semaglutide, further supports the transition toward biologically stratified hepatology. Although prospective validation remains necessary, the convergence of genetics, clonal biology, and targeted therapeutics suggests that MASLD is moving toward an era of precision medicine. - Source: PubMed
Publication date: 2026/07/24
Crespo JavierAlonso-Peña MartaJiménez-González CarolinaCayón-Gonzalez LorenaIruzubieta Paula - Lifestyle factors (i.e. obesity) worsen infertility in both sexes. Metabolic dysfunction-associated steatotic liver disease (MASLD) in particular and adverse metabolic profile in general seem to be related to infertility, for the relationship with the over-weight and the endocrinological dysregulation as in Polycystic Ovary Syndrome, erectile disfunction and hypogonadism. - Source: PubMed
Publication date: 2026/06/15
Aquino Carmen ImmaVercellino NicoleFortina ElisabettaFerrante DanielaRigamonti CristinaMinisini RosalbaPirisi MarioRemorgida ValentinoBellan MattiaSurico Daniela - Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized during adolescence and exhibits sex-specific characteristics. Its prevalence in late adolescent females is around 10% in the general population and exceeds 30% in obesity. Genetic variants in , , and modulate hepatic fat accumulation and liver injury in adults, but evidence in adolescent females remains limited. This study examined MASLD-related variants ( rs738409, rs641738, rs2642438) in relation to metabolic and immune-inflammation indices in a late-adolescent female cohort. A cross-sectional analysis was performed in a prospectively assembled female cohort ( = 150; age 16-19 years). Ultrasound-defined MASLD prevalence was 16.7%. Although genotype-wise differences did not reach statistical significance, MASLD prevalence was directionally higher among G- and T-allele carriers, while a non-uniform, directionally favorable pattern was observed for the A allele. Nominal, unadjusted differences were observed for low-density lipoprotein cholesterol (LDL-c) and systemic immune-inflammation index (SII) across . Cumulative risk-allele burden analyses identified nominal trends for triglycerides (K-W = 0.05; J-T = 0.014) and triglyceride-glucose (TyG) index (K-W = 0.034; J-T = 0.008), which were not retained after adjustment for age and body mass index. Overall, these findings indicate modest, exploratory genotype-related patterns in metabolic and hematological immune-inflammation indices within a relatively healthy, late-adolescent female population. TyG and SII exhibited substantial inter-individual variability but did not demonstrate independent predictive value. Larger, longitudinal studies with advanced imaging are required to clarify the role of genetic variation and simple hematological metabolic-inflammation indices in early MASLD risk assessment in adolescent females. - Source: PubMed
Publication date: 2026/05/27
Jurkovic Mlakar SimonaKlisic AleksandraMarc JanjaOstanek Barbara