Ask about this productRelated genes to: CYP2E1 antibody
- Gene:
- CYP2E1 NIH gene
- Name:
- cytochrome P450 family 2 subfamily E member 1
- Previous symbol:
- CYP2E
- Synonyms:
- -
- Chromosome:
- 10q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-03-03
- Date modifiied:
- 2015-12-09
Related products to: CYP2E1 antibody
Related articles to: CYP2E1 antibody
- The induction of cytochrome P450 2E1 (CYP2E1) and heme oxygenase-1 (HO-1) and reduction in their reciprocally regulated circadian clock protein Period 2 (Per2) contribute to ethanol (EtOH)-induced cardiac dysfunction in male rats. However, it remains unknown if these responses, which lead to ferroptosis (iron-dependent cell death), are sex-specific. These translational studies are crucial because women and female rats are more susceptible to EtOH-induced cardiac dysfunction, despite the biological estrogen (E2)-dependent upregulation of Per2 and dampening of ferroptosis in the heart. We hypothesize that CYP2E1 induction transforms E2 into a proinflammatory hormone that paradoxically suppresses Per2 and exacerbates ferroptosis, resulting in worsened EtOH-induced cardiac dysfunction in females. Female Sprague-Dawley rats (n = 6/group) underwent bilateral ovariectomy (OVX) and were assigned to OVX control, OVX + EtOH (5% w/v liquid diet), and OVX + EtOH + E2 (20 μg/kg) for 8 weeks. Cardiac function was assessed by echocardiography, followed by biochemical and molecular analyses. Compared to the OVX + vehicle or OVX + EtOH groups, the OVX + EtOH + E2 group exhibited significantly impaired cardiac function (reduced ejection fraction, fractional shortening). These functional alterations were linked to enhanced CYP2E1 activity and reduced Per2 expression. Further, histological analyses revealed myocardial architectural disruption and collagen deposition in the OVX + EtOH + E2 group. Together, these results suggest that EtOH alters E2 signaling, contributing to oxidative stress and ferroptosis-induced cardiac dysfunction in females. - Source: PubMed
Publication date: 2026/05/20
Ahmed Syed AneesAbdel-Rahman Abdel A - Rheumatoid arthritis (RA) is an autoimmune disease characterized by aberrant and persistent immune responses against self-antigens. However, the mechanisms of autoantibody production and the specific self-antigens in RA are not fully understood. CYP2E1 has been identified as a novel inflammatory target. It also exhibits immunogenicity and participates in autoimmune pathogenesis. Here, we explored the role of CYP2E1 in RA. In this study, we found that anti-CYP2E1 autoantibodies and CYP2E1 are elevated in RA and are closely related to inflammation and immunity. Cyp2e1 knockout protected RA rats against joint damage. Preclinical investigations further demonstrate that pharmacological inhibition of CYP2E1 by 1-(4-methyl-5-thiazolyl) ethenone (Q11) exhibits significant therapeutic efficacy in 3 RA animal models. Mechanistically, CYP2E1 inhibition attenuates inflammation by suppressing macrophage M1 polarization and exerts immunosuppressive effects via regulating the Th17/Treg balance. Our study identifies elevated anti-CYP2E1 autoantibodies in RA patients, advancing understanding of RA pathogenesis and providing a novel potential biomarker. Furthermore, we demonstrate that CYP2E1 inhibition ameliorates RA by regulating inflammation and immunity, providing a promising dual-targeting therapeutic strategy for RA. SIGNIFICANCE STATEMENT: This study identifies elevated anti-CYP2E1 autoantibodies in rheumatoid arthritis, revealing a previously unrecognized autoimmune target and potential biomarker. It further demonstrates that CYP2E1 inhibition alleviates disease by concurrently modulating inflammatory responses and immune balance, highlighting a promising dual-target therapeutic strategy. - Source: PubMed
Publication date: 2026/04/29
Gao LiyuanYang HongmingDeng MengyanHai XiaYang RuiTang LimingWen QiangXu HaiweiGao NaQiao Hailing - Prospective studies on meat intake and steatotic liver disease (SLD) risk, including its emerging subtypes and gene-diet interactions, are limited. - Source: PubMed
Publication date: 2026/05/19
Xu YangxinLiang ShaoxianLi MeilingChang YuChen JieQin XinshengCao HongjuanZhang ZhuangYang Wanshui - 2,5-Dimethylfuran (DMF) is a heat-induced contaminant found in various thermally processed foods. Due to its structural similarity to furan, a well-known hepatotoxin and potential human carcinogen, the presence of DMF in food poses a potential risk to consumers. DMF undergoes cytochrome P450 (CYP)-mediated biotransformation leading to the formation of two primary phase-I metabolites: the reactive cis-3-hexene-2,5-dione (HDO), which can react with cellular nucleophiles, and the primary alcohol 5-methylfurfuryl alcohol (MFA), formed after hydroxylation of the alkyl moiety. To deduce the in vitro formation kinetics of these two phase-I metabolites, we utilised a newly developed HPLC-ESI-MS/MS method to quantify HDO after scavenging with glutathione and monitored the formation of MFA by GC-MS in parallel. Metabolic activation and the formation of HDO was the predominant biotransformation pathway in human liver microsomes, whereas the parallel formation of MFA was significantly less efficient. In line with data on the metabolic activation of furan, CYP2E1 was the most active human CYP-isoform in the potential metabolic activation of DMF. However, CYP3A4 and CYP2D6 also contributed to the HDO formation in vitro. Hydroxylation of DMF and formation of MFA were exclusively catalysed by CYP2E1. Despite the formation of MFA as an alternative metabolic pathway, our kinetic data indicate that DMF is primarily metabolised by CYP2E1 to the reactive cis-enedial intermediate HDO, particularly at physiologically relevant concentrations. Therefore, exposure to DMF may contribute to the overall risk associated with dietary exposure to furans. - Source: PubMed
Publication date: 2026/05/20
Appel JonasKulosa CarolinBecker NicoStegmüller SimoneSadzik SullivanRichling Elke - Acetaminophen (APAP) exposures during human development are common. Emerging epidemiologic and experimental evidence links these exposures to subsequent pulmonary morbidity; however, the underlying mechanisms remain incompletely defined. Cell type-specific expression of the xenobiotic enzyme CYP2E1 is a critical determinant of susceptibility to APAP toxicity. CYP2E1-mediated formation of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) induces mitochondrial injury, which can trigger sterile inflammation through Toll-like receptor 9 (TLR9)-dependent innate immune signaling. The developing mouse lung is particularly vulnerable to APAP exposure at postnatal day 14 (P14), a time point within peak alveologenesis that coincides with maximal pulmonary CYP2E1 expression; however, the role of TLR9 signaling in this developmental window has remained unclear. In a preclinical model, wild-type (WT) and TLR9 knockout (TLR9 KO) male and female mice received a single, non-hepatotoxic dose of APAP (140 mg/kg, intraperitoneal) at P14. Acute lung injury occurred in both genotypes, but TLR9 deficiency reduced pro-inflammatory target gene () expression, and associated STAT3 activation and target gene () expression. Whereas APAP-exposed WT mice demonstrated persistent structural and functional abnormalities at P28, attenuation of the early inflammatory response in TLR9 KO mice preserved lung architecture and pulmonary function. These findings identify TLR9-dependent innate immune activation as a mechanistic link between early-life APAP exposure and impaired lung development. The data further suggest that limiting inflammation during the critical window of alveologenesis may preserve normal lung maturation and reduce later pulmonary morbidity. Further studies are warranted to define the clinical relevance these findings. - Source: PubMed
Publication date: 2026/05/19
Malyshkina AnastasiaSolar MackBalasubramaniyan NatarajanZheng LijunMcCulley David JMorro MusahSeymour CadenceSajti EnikoOrlicky David JSosa AlexanderSmith Bradford JWright Clyde J