Ask about this productRelated genes to: CYP7B1 antibody
- Gene:
- CYP7B1 NIH gene
- Name:
- cytochrome P450 family 7 subfamily B member 1
- Previous symbol:
- SPG5A
- Synonyms:
- -
- Chromosome:
- 8q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2018-02-28
Related products to: CYP7B1 antibody
Related articles to: CYP7B1 antibody
- : Based on previous findings on the Lingguizhugan (LGZG)-mediated gut-liver axis, this study clarifies the therapeutic mechanisms of LGZG in metabolic dysfunction-associated steatotic liver disease (MASLD), with a focus on the gut microbiota-bile acid-TGR5 (GPBAR1) axis. : C57BL/6J mice were fed a high-fat diet (HFD) for 8 weeks to induce MASLD, followed by 4-week LGZG intervention (21.57 g/kg/day, oral gavage). Metabolic phenotypes, gut microbiota (16S rRNA sequencing), serum/hepatic bile acids (targeted metabolomics), and molecular targets (qPCR/Western blot) were analyzed. : LGZG significantly alleviated HFD-induced obesity, insulin resistance, and hepatic steatosis, while enhancing whole-body energy expenditure (increased oxygen consumption (VO), and heat production ( < 0.05). It also reduced serum ALT ( < 0.001) and AST levels ( < 0.01). Mechanistically, LGZG remodeled the gut microbiota, specifically increasing , and _NK4A236_group while decreasing . This shift inhibited the intestinal FXR-Fgf15 axis, concurrently activating the hepatic alternative bile acid synthesis pathway (upregulating CYP27A1 and CYP7B1 protein expression; < 0.001 and < 0.01, respectively). Consequently, systemic accumulation of non-12α-hydroxylated bile acids (non-12-OH BAs) such as hyocholic acid (HCA) and 7-ketolithocholic acid (7-ketoLCA) occurred-known TGR5 agonists and intestinal FXR antagonists. These changes elevated serum GLP-1 levels ( < 0.05) and activated adipose TGR5-cAMP/PKA/CREB signaling. The metabolic benefits primarily originated from non-12-OH BAs enrichment and TGR5-mediated adipose browning, not hepatic FXR activation. : Our findings show that LGZG ameliorates MASLD by remodeling bile acid profiles via intestinal FXR-Fgf15 axis inhibition and hepatic alternative synthesis pathway activation. This study highlights the TGR5-targeting properties of LGZG, providing a mechanistic basis for its therapeutic use in metabolic disorders. - Source: PubMed
Publication date: 2026/03/24
Sun Yun-HongDing Pei-LunWang XueWang Yi-RongZhu Ming-ZheWang KaiDai LiangDang Yan-QiJi GuangLi MengZhou Wen-Jun - Bile acids, the primary constituents of mammalian bile, are synthesized in the liver from cholesterol and secreted into the intestine to perform essential physiological functions. Primary bile acid synthesis is the principal pathway for cholesterol catabolism and whole-body cholesterol homeostasis, occurring predominantly via the classical and alternative pathways. To elucidate the effects of altitude on serum bile acid profiles and synthesis pathways in SD rats, this study utilized UPLC-MS/MS to analyze serum bile acid composition in animals housed at high and low altitudes. Additionally, qRT-PCR and Western blotting assessed mRNA transcription and protein expression of key genes involved in primary bile acid synthesis in the liver and intestinal tissues (ileum, duodenum, and colon). Results showed that serum levels of total and primary bile acids significantly decreased with increasing altitude. Furthermore, hepatic mRNA and protein expression of , , , and were significantly downregulated. mRNA expression in the liver, ileum, duodenum, and colon was significantly decreased with increasing altitude. Meanwhile, the protein expression of both FGF15 and SHP showed a downward trend, with a significant decrease for FGF15 and a non-significant decrease for SHP. These findings suggest that primary bile acid synthesis in SD rats is dominated by the classical pathway. As altitude increases, bile acid synthesis in SD rats is significantly inhibited, indicating that high-altitude hypobaric hypoxia is the primary inhibitory factor. This study provides critical data for elucidating the adaptive mechanisms of bile acid metabolism in mammals exposed to high-altitude hypoxia, thereby establishing a theoretical foundation for investigating the regulation of host lipid metabolism influenced by such conditions. - Source: PubMed
Publication date: 2026/04/10
Ma PiaoHu QingfeiMa FanZhang WenjuanGu HaifengWei DengbangAn Zhifang - The incidence of inflammatory bowel disease (IBD) is notably increased in patients with nonalcoholic fatty liver disease (NAFLD). The high-fat diet (HFD), a common dietary intervention linked to NAFLD development, disrupts intestinal homeostasis and exacerbates colitis. However, the underlying mechanisms remains unknown. We hypothesized that hepatic lipid metabolism contributes to IBD pathogenesis via disruption of the liver‑gut axis. Here, we established a dextran sulfate sodium (DSS)-induced colitis in mice fed with HFD and investigated the mechanisms by which HFD exacerbates colitis. Our results revealed that an HFD markedly reduced intestinal barrier proteins (Claudin1, E-cadherin) and notably increased Escherichia coli levels. Furthermore, it upregulated the hepatic enzyme Cyp7b1 and suppressed key colonic autophagy markers (LC3-II, Beclin1, ATG5), while elevating P62. An approach combining data available in public domain and in-house RNA-seq revealed a significant correlation between hepatic Cyp7b1 and colonic autophagy. Treatment with Cyp7b1-derived chenodeoxycholic acid (CDCA) led to decreased levels of Claudin1, Occludin, LC3-II, Beclin1, and ATG5, accompanied by an increase in P62, suggesting that CDCA impairs both the epithelial barrier and autophagic flux in the colon. In conclusion, our findings indicated that HFD exacerbated colitis by upregulating hepatic Cyp7b1, which in turn suppresses colonic autophagy and promotes IBD pathogenesis. These findings contribute to a deeper understanding of the NAFLD‑IBD interplay and provide novel mechanistic insights for targeted therapeutic strategies in patients with NAFLD and IBD. - Source: PubMed
Publication date: 2026/04/28
Xu TianShi JuanJi JingMa ChongyangLi Jingnan - Chemotherapeutic resistance remains a major contributor to tumor recurrence and unfavorable clinical outcomes in colorectal cancer (CRC). Although cholesterol metabolic reprogramming has been implicated in tumorigenesis, metastasis, and drug resistance across multiple malignancies, its specific role in CRC chemoresistance requires systematic investigation. We analyzed RNA-seq data from GEO dataset GSE196900 to identify differentially expressed genes (|Log2FC| ≥ 1.5, adjusted < 0.05). Functional enrichment analysis (GO/KEGG), protein-protein interaction (PPI) network construction, and gene set enrichment analysis (GSEA) were performed. Experimental validation using 5-fluorouracil (5-FU)-resistant CRC cell lines (HCT8/HCT15) included cholesterol/25-hydroxycholesterol (25-HC) treatments, assessed through CCK-8 proliferation assays, wound healing migration tests, quantitative real-time PCR (qRT-PCR), Western blotting, and cholesterol metabolite quantification. Integrative bioinformatics and experimental evidence revealed that 5-FU-resistant CRC cells demonstrate significant upregulation of cholesterol metabolism regulators, including lectin-type oxidized LDL Receptor 1 (LOX1), cholesterol 25-hydroxylase (CH25H), and Cytochrome P450 Family 7 Subfamily B Member 1 (CYP7B1). These cells exhibited impaired cholesterol efflux capacity and consequent intracellular cholesterol accumulation. Exogenous supplementation with cholesterol or 25-HC promoted proliferation, migration, and chemoresistance in both parental and resistant cells. Conversely, CH25H knockdown in resistant cells significantly attenuated malignant phenotypes and restored drug sensitivity. Our findings establish cholesterol metabolic dysregulation as a novel mechanistic contributor to 5-FU resistance in CRC, mediated through the LOX1-CH25H-CYP7B1 regulatory axis. These results propose that therapeutic targeting of cholesterol homeostasis may overcome chemoresistance and improve clinical management of refractory CRC patients. - Source: PubMed
Publication date: 2026/04/25
Cheng HaixiaHuang LuyaoHuang JieshenFeng JiashengHuang KehuaLiu MeiLi Ji - Macrophages play a key role in kidney inflammation and fibrosis. The oxysterol receptor G protein-coupled receptor 183 (GPR183) is an important immunomodulatory receptor, but its role in kidney disease is undefined. In this study, we investigated the contribution of GPR183 to renal injury using adenine diet-induced chronic kidney disease and folic acid-induced nephropathy models. Both models exhibited marked upregulation of the cholesterol hydroxylases CH25H and CYP7B1, along with increased GPR183 expression in the kidney. Immunofluorescence analysis demonstrated that GPR183 colocalized with M1 macrophage markers within injured kidneys. Genetic deletion of GPR183 selectively reduced renal M1 macrophage accumulation and proinflammatory cytokine expression without affecting M2 macrophage infiltration, leading to improved renal function. GPR183 deficiency also significantly attenuated renal fibrosis, as evidenced by decreased collagen deposition and reduced expression of fibronectin and α-smooth muscle actin. In primary bone marrow-derived macrophages, GPR183 deletion suppressed lipopolysaccharide (LPS) and interferon γ (IFN-γ)-induced M1 polarization through inhibition of NF-κB signaling. Finally, analysis of publicly available human single-cell RNA sequencing data demonstrated substantial GPR183 expression in immune cells, including macrophages, in patients with chronic kidney disease. These findings identify GPR183 as a key regulator of macrophage phenotype in kidney injury and demonstrate that activation of the oxysterol-GPR183 axis promotes inflammatory and fibrotic renal remodeling. Targeting GPR183 may therefore represent a novel therapeutic strategy for the treatment of progressive kidney disease. This study identifies GPR183 as a previously unrecognized regulator of macrophage polarization and renal fibrogenesis. We demonstrate that kidney injury activates an oxysterol-GPR183 signaling axis that promotes NF-κB-dependent M1 macrophage polarization. Genetic deletion of GPR183 selectively limits inflammatory macrophage accumulation, attenuates fibrosis, and preserves renal function, establishing GPR183 as a novel therapeutic target in progressive kidney disease. - Source: PubMed
Publication date: 2026/04/09
Zhang QianWang YanFan YuHan Seung SeokXie HanRhee Eugene PWen Donghai