Ask about this productRelated genes to: FGF19 protein
- Gene:
- FGF19 NIH gene
- Name:
- fibroblast growth factor 19
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-06
- Date modifiied:
- 2016-10-05
Related products to: FGF19 protein
Related articles to: FGF19 protein
- Metabolic dysfunction-associated steatotic liver disease (MASLD) and its inflammatory-fibrotic phenotype (MASH) exhibit pronounced immunometabolic coupling. This review synthesizes evidence along the gut-liver axis, from epithelial tight-junction and gut vascular barrier (GVB) failure to TLR4-MyD88/TRIF-NF-κB amplification and NLRP3 inflammasome activation and outlines the logic of the gut-derived exposure spectrum-lipopolysaccharide (LPS), endogenous ethanol, bile acids (BAs), short-chain fatty acids (SCFAs), and trimethylamine N-oxide (TMAO). We position BA-FXR/TGR5, SCFAs-GPR41/43, and AMPK/Nrf2 as upstream/downstream modulators that reset inflammatory thresholds and confer stage-dependent druggability. Based on node-to-pathway mapping, we summarize mechanisms and translational signals for berberine (BBR), Qushihuayu (QSHY), Da-Chai-Hu Decoction (DCHD), and polysaccharides (e.g., Astragalus, Ganoderma), emphasizing pharmacokinetic and site-of-exposure constraints that support "gut-first" actions. We propose a minimal companion biomarker set-LBP/sCD14, BA profiles with FGF19-C4 dynamics, and IL-1β/GSDMD-N-paired with hierarchical imaging gates (≥30% relative MRI-PDFF decline; MRE/ELF) to underpin response typing and go/no-go decisions. Finally, we highlight critical gaps (direct human GVB readouts; longitudinal multi-omics bridged to clinical outcomes) and outline a biomarker-driven multi-arm multi-stage (MAMS) pathway for adaptive, stratified development of multi-target traditional medicine interventions in MASLD/MASH. - Source: PubMed
Publication date: 2026/04/17
Ren LianjieHe QinHu ZhuyuanJin JinjinTao Feibao - Copy number variation (CNV), including genomic gains or losses of DNA segments ranging from kilobases to megabases, represents a major source of genetic diversity and can substantially alter gene dosage, regulation, and phenotype. Although CNVs have been catalogued across many dog breeds in prior large-scale efforts, breed-specific CNVs, defined as copy-number changes that are highly prevalent within one breed but rare or absent across others, have not been systematically investigated. To address this gap, we analyzed whole-genome sequencing data from 436 dogs representing 105 modern breeds and constructed a high-resolution catalog of breed-specific CNVs. - Source: PubMed
Publication date: 2026/04/27
Wang ShiyingLi ZichengBargmann WalkerChen ZhiyuanGruen JefferyHoh Josephine - Bile acid diarrhea (BAD) is an underrecognized cause of chronic diarrhea that makes a significant contribution to the symptom burden and impaired quality of life. Despite increasing awareness, BAD is frequently misdiagnosed as diarrhoea-predominant irritable bowel syndrome (IBS-D), leading to delayed diagnosis and incomplete symptom control. Current management relies primarily on bile acid sequestrants, which are effective for many patients but limited by poor tolerability, variable adherence, and incomplete response in a subset, prompting interest in alternative therapeutic approaches targeting bile acid dysregulation. Advances in understanding enterohepatic signaling have highlighted the role of the farnesoid X receptor-fibroblast growth factor 19 (FXR-FGF19) axis in regulating bile acid synthesis, secretion, and motility. In parallel, glucagon-like peptide-1 (GLP-1) receptor agonists, which are commonly used in the treatment of metabolic diseases, affect gastrointestinal motility, secretion, and neurohormonal signaling by mechanisms that overlap with those that are implicated in BAD. Emerging clinical studies, including randomized trials comparing GLP-1-based therapy with established bile acid sequestrants, have begun to explore their potential role in BAD, although the current evidence base remains limited and investigational. This narrative review synthesizes peer-reviewed evidence examining the biological rationale, diagnostic context, and clinical data relevant to GLP-1 receptor agonists in BAD. Literature was identified primarily by PubMed/Medical Literature Analysis and Retrieval System Online (MEDLINE) searches supplemented by manual screening of reference lists of key reviews and clinical studies and integrated narratively because of heterogeneity of study design, exposure definitions, and outcome measures. Current evidence suggests that GLP-1 receptor agonists represent a biologically plausible area of investigation for selected patients with persistent symptoms despite standard therapy. This review does not advocate routine clinical use but aims to contextualize emerging BAD-specific and mechanistic data to inform hypothesis generation, patient selection, and future research. Available data are still limited, and GLP-1 receptor agonists have not been established as a treatment for BAD. Further prospective studies with standardized outcomes are needed to clarify their role and inform evidence-based clinical practice. - Source: PubMed
Publication date: 2026/03/24
Omeludike Eunice KNwabueze Cherechi OUbah NneomaOkeke NzubechukwuAregbesola EuniceOnyiaorah Chimezie RIgbokwe Mesoma AGujral MeherLawal Ridwan AAkande Yetunde F - Fibroblast growth factor (FGF)-fibroblast growth factor receptor (FGFR) signaling constitutes a fundamental regulatory network governing epithelial turnover, metabolic homeostasis, and immune modulation across the gastrointestinal tract. Although discrete FGF pathways have been intensively investigated in inflammatory bowel disease, hepatobiliary disorders, and gastrointestinal malignancies, how these signaling programs are coordinated across pathological contexts remains insufficiently resolved. In this review, we integrate evidence from human cohorts, experimental systems, and clinical studies to conceptualize the FGF-FGFR axis as a context-dependent metabolic-barrier-immune rheostat. Paracrine activation of epithelial FGFR2b supports mucosal restitution and barrier re-establishment following injury, whereas endocrine FGFs-including FGF19, FGF21, and FGF23-couple bile acid signaling, systemic metabolic stress, and mineral balance to intestinal and hepatic inflammatory responses. Perturbation of these adaptive signaling circuits contributes to persistent inflammation and is frequently co-opted by oncogenic events, such as FGFR2b amplification, FGFR2 gene fusions, and aberrant FGF19-FGFR4 activation, during gastrointestinal tumorigenesis. Framing the FGF-FGFR network as an integrated rheostat offers a unifying mechanistic paradigm that links epithelial damage, metabolic dysregulation, and cancer development. It underscores the need for context-selective therapeutic interventions that reconcile tissue repair with long-term oncogenic risk. - Source: PubMed
Publication date: 2026/03/26
Saad Khamis Salem SaeedZhou ChunfangLu GuangxinWei GangCha HuolongAlwabri EzzaddinZhang ZhifangSun ZequnLiao Yingying - Anaplastic lymphoma kinase () rearrangement has been identified in approximately 1% of lung squamous cell carcinomas (LUSCCs). Due to its rarity, the efficacy of anaplastic lymphoma kinase-tyrosine kinase inhibitors in the treatment of -positive LUSCCs is poorly characterized. - Source: PubMed
Publication date: 2026/03/24
Li ShengshuDu XiaosongZhang XinxinMa HaixiaYang YanliLi YuanWei QinChen YanLi HongweiBu PengLiu DujuanHan SongyanChen Deyi