HMOX1 Antibody
- Known as:
- HMOX1 Antibody
- Catalog number:
- 32266
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- HMOX1 Antibody
Related genes to: HMOX1 Antibody
- Gene:
- HMOX1 NIH gene
- Name:
- heme oxygenase 1
- Previous symbol:
- -
- Synonyms:
- bK286B10, HO-1
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-15
- Date modifiied:
- 2017-12-15
Related products to: HMOX1 Antibody
Related articles to: HMOX1 Antibody
- Intrahepatic cholangiocarcinoma is a highly lethal malignancy characterized by a rising incidence and a dismal 5-year survival rate of < 10%. While targeted therapies and immunotherapies have expanded treatment paradigms, their clinical efficacy remains hampered by modest patient response rates. Here, we identify total glucosides of paeony and its principal bioactive monomer, paeoniflorigenone (PFG), as potential effective therapeutic agents against ICC, demonstrating potent suppression of malignant phenotypes across multi-dimensional ICC models. Transcriptomic profiling identified ferroptosis as the primary mechanism driving PFG-induced ICC cell death, which is hallmarked by intracellular Fe²⁺ overload, robust ROS generation, and lipid peroxidation. Mechanistically, PFG directly binds to TRIM28, triggering its phosphorylation at Ser824. This modification alleviates repressive H3K9me3 occupancy at the HMOX1 promoter, thereby unlocking local chromatin accessibility to drive HMOX1 transcription and culminate in ferroptosis. Notably, PFG-induced ferroptosis not only curbs ICC cell proliferation and migration but also activates antigen presentation and reshapes a tumoricidal immune microenvironment, characterized by enhanced infiltration and activation of CD8⁺ cytotoxic T cells. In summary, this study unveils a previously unrecognized ferroptosis regulatory pathway-the TRIM28/H3K9me3/HMOX1 axis-and demonstrates that PFG may represent a potential natural small-molecule candidate for ICC treatment. - Source: PubMed
Publication date: 2026/09/27
Lin KainanLu YunkunLin ZhihaoDou JieWang QianqianLiu YangJia XingLi YuanqiangYu XuefeiWang DanqingLi QinglinCai XiujunJin Renan - Excessive exposure to UVB can induce inflammatory responses and oxidative stress, leading to skin damage. Peony seed oil is rich in unsaturated fatty acids and has been reported to possess anti-inflammatory and antioxidant properties. This study investigated the protective effects and underlying mechanisms of Paeonia delavayi seed oil (PDSO) against UVB-induced damage in human keratinocytes. PDSO at 30-120 μg/mL attenuated UVB-induced inflammation by reducing the mRNA expression of TNF, IL6, CXCL8, and PTGS2 and suppressing the secretion of IL-6 and IL-8. PDSO also inhibited UVB-induced activation of NF-κB signaling. Regarding oxidative stress, 120 μg/mL PDSO reduced intracellular ROS production, decreased MDA levels by approximately 29.4%, and increased SOD activity by approximately 122.0% compared with the UVB group. PDSO also increased the mRNA expression of antioxidant-related genes, including NFE2L2, HMOX1, SOD1, CAT, GCLC, and GCLM. In addition, PDSO alleviated the UVB-induced reduction in keratinocyte viability and attenuated photoaging-related changes. Transcriptomic analysis identified PI3K/Akt signaling as a candidate pathway associated with PDSO treatment, and western blotting further showed that PDSO inhibited UVB-induced PI3K/Akt signaling. Pharmacological intervention with the PI3K activator 740YP partially reversed the anti-inflammatory effects of PDSO, whereas LY294002 exerted anti-inflammatory effects and further enhanced those of PDSO. Moreover, oleic acid and linolenic acid alleviated UVB-induced inflammation and oxidative stress. Collectively, PDSO protects keratinocytes against UVB-induced damage, with PI3K/Akt and NF-κB signaling contributing to its protective effects. - Source: PubMed
Publication date: 2026/09/26
Wang RencongXu PengZhang YindiJin XiaoliZhao ZiyanQu LipingWang Feifei - Skin fibrosis is a chronic inflammatory disorder characterized by excessive extracellular matrix (ECM) deposition and aberrant fibroblast activation, leading to tissue stiffening and progressive functional impairment. Despite its clinical prevalence, no FDA-approved therapies are currently available, highlighting a significant unmet medical need. The present study investigated the anti-fibrotic potential of yohimbine using an integrated network pharmacology approach and a bleomycin (BLM)-induced murine skin fibrosis model. Network pharmacology identified 168 overlapping targets between yohimbine and skin fibrosis, while KEGG enrichment highlighted the PI3K/Akt and MAPK pathways as key antifibrotic signaling mechanisms. Subcutaneous administration of BLM (3 mg/kg) for 28 days induced marked skin fibrosis compared with sham control. Yohimbine treatment at 2.5 and 5 mg/kg attenuated bleomycin (BLM)-induced skin fibrosis, with the 5 mg/kg dose demonstrating a more consistent antifibrotic response compared with the BLM group. Molecular analyses demonstrated that yohimbine suppressed the pro-fibrotic (Ccn2, α-Sma, Vimentin, Zeb, and Snail) and inflammatory markers (Tnf-α) expression. Furthermore, yohimbine restored the expression of antifibrotic (Hgf) and antioxidant (Gstp1, Nrf2, and Hmox1) markers, while reducing ECM-associated markers, including Fibronectin (FN1) and Collagen Type III (COL3α1), at both mRNA and protein levels. Histopathological, Masson's trichrome, and Sirius red/fast green collagen staining analysis further demonstrated that yohimbine treatment significantly (p < 0.05) reduced collagen deposition and restored normal skin architecture. Collectively, these findings demonstrate that yohimbine attenuates skin fibrosis by suppressing inflammatory and fibrotic responses, potentially through modulation of PI3K/Akt-MAPK signaling, and may represent a potential lead for further investigation in fibrotic skin disorders. - Source: PubMed
Publication date: 2026/09/26
Eedara AbhisheikS JeyasankariChandra YogeshKathirvel MuralidharanAndugulapati Sai Balaji - Drug-induced liver injury (DILI) presents a significant clinical challenge with limited preventive and therapeutic options. Artesunate (ART) holds potential for DILI treatment; however, its precise hepatoprotective mechanisms and direct molecular target(s) remain unclear. - Source: PubMed
Publication date: 2026/09/21
Wei MingyueHe JunjieZhang YanzhaoChen HetaoWang XueLiu MiaomiaoChang JianyingFan ChunyangJiang HongweiLiu Chuanxin - Oral Xuesaitong soft capsules have been reported to improve functional outcomes after ischemic stroke, but their molecular mediators remain uncertain. We evaluated human genetic support for pharmacology-informed saponin-related candidate genes. A targeted pharmacological audit was followed by cis-QTL Mendelian randomization (MR) and regional colocalization using GISCOME outcomes. The severity-adjusted ordinal modified Rankin Scale (mRS) was primary. Eleven CKLF, KMO, and MT2A gene-tissue hypotheses formed the eQTL testing family; HMOX1 and OGA underwent pQTL analyses. A 13-test Bonferroni sensitivity calculation combined these hypotheses. Colocalization required PP.H4 ≥ 0.80. KMO analyses covered 15 GTEx tissues, three outcomes, and two external eQTL datasets. The summary-statistics study was not prospectively registered. The audit identified 29 component-protein relations involving 19 proteins. Further, 7 of 11 eQTL hypotheses were harmonized. Higher genetically predicted KMO expression in whole blood was associated with better ordinal mRS (β = -0.906; 95% CI, -1.521 to -0.290; = 0.0039; adjusted = 0.043 for 11 tests and 0.051 for 13 tests). HMOX1 and OGA MR estimates were nonsignificant. Primary PP.H4 values were 0.033, 0.027, and 0.535 for HMOX1, OGA, and KMO, respectively. None of the 45 GTEx or six external comparisons met the criterion under primary priors. No candidate met the joint MR and colocalization criterion. KMO significance was sensitive to multiplicity and standard-error specification, while colocalization support was insufficient and prior-sensitive. These findings do not establish a therapeutic target or test the efficacy of oral Xuesaitong. - Source: PubMed
Publication date: 2026/09/20
Deng GuoliangCui TongXu YifengGao WanningLi NanJiang LijuanZhang Wenfeng