Ask about this productRelated genes to: CYP2J2 antibody
- Gene:
- CYP2J2 NIH gene
- Name:
- cytochrome P450 family 2 subfamily J member 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-21
- Date modifiied:
- 2016-10-05
Related products to: CYP2J2 antibody
Related articles to: CYP2J2 antibody
- Menopause is associated with a marked increase in cardiac hypertrophy and progression to heart failure with preserved ejection fraction (HFpEF), a condition that disproportionately affects women and lacks effective targeted therapies. Although estrogen deficiency has long been implicated in postmenopausal cardiac remodeling, emerging evidence highlights a critical role for cytochrome P450 (CYP)-derived arachidonic acid metabolites as central regulators of myocardial structure and function. In a healthy premenopausal heart, a balance between cardioprotective epoxyeicosatrienoic acids (EETs), produced by the CYP2J2 and CYP2C enzymes, and the pro-hypertrophic metabolite 20-hydroxyeicosatetraenoic acid (20-HETE), produced by the CYP4A and CYP4F isoforms, supports adaptive remodeling and diastolic function. Menopause disrupts this equilibrium by estrogen-mediated reprogramming of CYP expression and activity, leading to diminished EET bioavailability, heightened 20-HETE signaling, and accelerated EETs breakdown by soluble epoxide hydrolase (sEH). This metabolic shift induces oxidative stress, calcium imbalance, fibroblast activation, extracellular matrix buildup, and cardiomyocyte enlargement, which together lead to ventricular stiffness and diastolic failure. This review aims to consolidate contemporary experimental and translational evidence linking CYP-derived eicosanoids to menopause-related cardiac hypertrophy and to assess novel non-hormonal therapeutic approaches, including sEH inhibitors, stable EET analogs, and CYP4A/20-HETE inhibitors, that target these molecular pathways. Targeting CYP-derived metabolites represents a promising mechanism-based approach to prevent or reverse postmenopausal cardiac hypertrophy and to modify the natural history of HFpEF. Importantly, these non-hormonal strategies may offer a safer therapeutic alternative to hormone replacement therapy by avoiding the systemic risks associated with exogenous estrogen exposure while directly targeting disease-specific molecular pathways. - Source: PubMed
Publication date: 2026/05/12
Abd El-Aziz Mostafa KShalaby Ali HEl-Mahrouk Sara REl-Kadi Ayman O S - Direct oral anticoagulants (DOACs) exhibit considerable individual variability in effectiveness and bleeding risk, possibly due to genetic differences. This study assessed how genetic polymorphisms impact the pharmacokinetics (PK) and outcomes of DOACs. - Source: PubMed
Publication date: 2026/04/14
Chai HuaruHuo JianiChen Hao - Tongue squamous cell carcinoma (TSCC) is clinically heterogeneous, and patients with a similar TNM stage can experience markedly different outcomes. We systematically reviewed omics-driven studies to identify prognostic TSCC biomarkers. Although fundamentally prognostic, we discussed their theoretical translational relevance regarding future clinical decisions-such as treatment stratification or surveillance intensity-while strictly framing them as preliminary, hypothesis-generating targets. PubMed, Scopus, Web of Science, and Cochrane were searched for original human studies published between 2014 and 2024 using high-throughput genomic or transcriptomic profiling. Study selection followed referred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), data were extracted with a structured workbook, and risk of bias was assessed using QUIPS and PROBAST, with reporting completeness appraised using REMARK. Seventeen studies were included, identifying 85 distinct biomarkers. Across biomarkers supported by multivariable overall survival analyses, higher-risk associations were reported for , , , , and , whereas lower-risk associations were reported for , , , , and . Recurrent biological themes included IL-17 signaling, ECM-receptor interaction, and focal adhesion. was the only biomarker reported in more than one included study, supporting its prioritization for validation. Although the evidence remains heterogeneous and largely hypothesis-generating, these markers may support the future validation of response-oriented therapeutic stratification in TSCC. - Source: PubMed
Publication date: 2026/04/10
Astreidis IoannisKostidis IliasMalousi AndigoniParaskevopoulos KonstantinosAndreadis DimitriosVahtsevanos KonstantinosVizirianakis Ioannis - The cytochrome P450 (P450 or CYP) superfamily, while extensively recognized for xenobiotic metabolism, is also critically involved in the biosynthesis of lipid mediators from polyunsaturated fatty acids (PUFAs). Distinct from cyclooxygenase (COX) and lipoxygenase (LOX) pathways, P450 enzymes uniquely catalyze the metabolism of PUFAs such as arachidonic acid (AA), to epoxy fatty acids (EpFAs), such as epoxyeicosatrienoic acids (EETs) and mid-chain or ω-terminal hydroxyeicosatrienoic acids (HETEs). Eicosanoid biosynthesis is initiated by phospholipase A (PLA)-mediated release of PUFAs from cellular membranes. Members of the CYP1-CYP4 subfamilies, including prominent human isoforms like CYP2C8, CYP2C9, and CYP2J2, exhibit significant epoxygenase activity, yielding regio- and stereo-specific EETs. These P450-derived oxylipins exert diverse physiological effects, influencing critical processes such as vascular tone, inflammation, angiogenesis, and ischemia-reperfusion injury. Their biological actions are often modulated by soluble epoxide hydrolase (sEH) and microsomal epoxide hydrolase (mEH), which hydrolyze EETs to less active dihydroxyeicosatrienoic acids (DHETs). Furthermore, P450s metabolize other PUFAs, including linoleic acid (LA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), generating distinct EpFAs with varying biological effects. Understanding the complex interplay of P450 isoforms, their substrate preferences, and the subsequent metabolic fates of their products is crucial for elucidating their functional roles in health and disease. - Source: PubMed
Publication date: 2025/10/14
Edin Matthew LGraves Joan PZeldin Darryl C - Clinically used drugs can adversely affect cardiac function. Doxorubicin (DOX), a chemotherapeutic drug, and efavirenz (EFV), an antiretroviral drug, are known to associate with adverse cardiovascular events and alterations of serum lipid profiles. In the heart, lipids serve as the main energy source and act as signaling molecules. Moreover, CYP2J2, a primary cytochrome P450 enzyme in the heart, metabolizes arachidonic acid. Drugs could alter the activity of CYP2J2, thereby modulating the levels of arachidonic acid. However, the effect of the above drugs on cardiac lipids is not fully elucidated. We hypothesized that DOX and EFV perturb endogenous lipid metabolism in heart tissues. In this work, we investigated lipid alterations in murine hearts following the above drug treatments using matrix-assisted laser desorption/ionization mass spectrometry imaging, which revealed region-specific localization of phosphatidylcholine (PC) and sphingomyelin (SM) in mouse heart tissues. Lipid molecules PC(34:2), PC(34:1), PC(32:0), and SM(37:1) showed alterations within mouse heart tissue in response to DOX treatment. Interestingly, hexosylceramide (42:2;O2), SM(40:2), and SM(40:3) showed increased abundance in the left ventricle of EFV-treated heart tissues relative to the control group. Notably, arachidonic acid, a precursor of various bioactive lipid mediators, was detected to be more abundant in drug-treated heart tissues as compared with controls. Proteomic analysis further demonstrated altered expression of cardiac proteins in response to drug treatments. The findings from in vitro inhibition assays suggest that EFV inhibits microsomal CYP2J2. Altogether, our results reveal the localized alterations of lipids in murine heart tissues following DOX and EFV treatments. SIGNIFICANCE STATEMENT: Clinically used drugs such as doxorubicin and efavirenz are known to associate with adverse cardiovascular events. Lipids play important roles in the cardiac function and both doxorubicin and efavirenz cause alterations of serum lipid levels. Using mass spectrometry imaging and bottom-up proteomics, we demonstrate the local region-specific alterations of phosphatidylcholine, sphingomyelin, hexosylceramide, and arachidonic acid in response to the above drugs in mouse heart tissues. Further, we performed in vitro inhibition assays to assess CYP2J2 inhibition by efavirenz. - Source: PubMed
Publication date: 2026/03/24
Jayasekera NimaleePhulara Nav RajTang Lloyd Wei TatRivas Anderson AlbertoSeneviratne Herana Kamal