Ask about this productRelated genes to: FGF21 protein
- Gene:
- FGF21 NIH gene
- Name:
- fibroblast growth factor 21
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2014-11-18
Related products to: FGF21 protein
Related articles to: FGF21 protein
- Intracerebral hemorrhage (ICH) is a neurological disorder characterized by a high mortality rate for which there is currently no definitive cure. Research has demonstrated that adipose-derived mesenchymal stem cells (ASCs) exhibit considerable potential in treating ICH. However, the advanced age of ICH patients and the necessary cell expansion before transplantation therapy could result in the senescence of ASCs, thereby compromising their viability and therapeutic efficacy. This study aims to investigate whether FGF21 (fibroblast growth factor 21) can rejuvenate aged ASCs by enhancing macroautophagy/autophagy flux and subsequently enhance the therapeutic efficacy of ICH. We demonstrated that the autophagy flux of aged ASCs was significantly decreased and FGF21 treatment significantly reversed the senescence phenotype and increased the viability of aged ASCs. Mechanistically, our findings suggested that FGF21 rejuvenates aged ASCs by augmenting autophagy flux, a process partly mediated by TFE3 (transcription factor E3) nuclear translocation. The FGF21-induced TFE3 nuclear translocation was partially facilitated potentially via the FGFR1-SIRT1-MTOR pathway. In addition, FGF21 enhanced the potential of senescent ASCs to differentiate into neurons. In the in vivo study, we further verified that FGF21 could enhance the therapeutic effect of ASCs on acute ICH rats. In conclusion, these results indicated that FGF21 could restore ASC viability by upregulating TFE3-mediated autophagy flux in part through the FGFR1-SIRT1-MTOR signaling pathway, enhanced the potential to improve the differentiation of ASCs into neural stem cells and enhanced the therapeutic effect of ASCs transplantation in acute ICH.: FGF21: fibroblast growth factor 21; TFE3: transcription factor E3; TFEB: transcription factor EB; DMEM: Dulbecco's modified Eagle medium; RAPA: rapamycin; 3-MA: 3-methyladenine; CQ: chloroquine; DMSO: dimethyl sulfoxide; RT-qPCR: quantitative real-time PCR; pAb: polyclonal antibody; mAb: monoclonal antibody; LAMP1: lysosomal associated membrane protein 1; SQSTM1/p62: sequestosome 1; MAP1lc3/LC3: microtubule associated protein 1 light chain 3; GFAP: glial fibrillary acidic protein; MAP2: microtubule associated protein 2; SOX2: SRY-box transcription factor 2; MOI: multiplicity of infection; FGFR1: fibroblast growth factor receptor 1; SIRT1: sirtuin 1; MTOR: mechanistic target of rapamycin kinase; ROS: reactive oxygen species; siRNA: small interfering RNA; OD: optical density; SASP: senescence-related secretion phenotype; IL6: interleukin 6; IL1B/IL-1β: interleukin 1 beta; TNF/TNF-α: tumor necrosis factor; CCL2/MCP-1: C-C motif chemokine ligand 2; BDNF: brain derived neurotrophic factor; VEGF: vascular endothelial growth factor; ICH: intracerebral hemorrhage; MLPT: modified limb placement test. - Source: PubMed
Publication date: 2026/05/19
Song BeiLiu ChengyunHu JingqiongZhao XiaofangFan HaohuiLiu TingGao GuangyuZhang XinyueGuang XuekeZhou QuanWang KunLu Weilin - Ultra-processed diets are associated with excessive energy intake, but studies examining the role of alcohol have produced conflicting results, despite the high energy density of ethanol. We constructed a mechanistic-ecological model to explain this inconsistency and tested its predictions using population dietary data. The model builds on experimentally established mechanisms to predict that, whereas alcohol will contribute ethanol calories irrespective of diet, its impact on total macronutrient energy intake varies depending on dietary pattern. Alcohol consumption stimulates FGF21, a hormone that increases savory (umami) preference and reduces sweet preference. In minimally processed food environments-where umami flavor is a relatively reliable indicator of protein in foods-umami-seeking should direct consumers toward satiating, high-protein foods, with limited effect on macronutrient energy intake. In contrast, on diets rich in ultra-processed savory foods and/or high-fat unprocessed meats, the correlation between umami flavor characteristics and protein is broken by umami-flavored low-protein foods (protein decoys), so alcohol instead drives dietary protein dilution and, through attenuated protein satiation, increased food and macronutrient energy intake (protein leverage). Mixture analysis paired with nutritional geometry confirmed these predictions in population data, suggesting the model may generalize to ecological contexts. Our results potentially explain why alcohol has variable effects on energy balance across dietary patterns and suggest that it exacerbates the obesogenic effects of ultra-processed diets-a potentially important interaction given their global rise. - Source: PubMed
Publication date: 2026/05/19
Grech AmandaSimpson Stephen JRaubenheimer David - Macrophage dysfunction serves as a pivotal factor in the delayed healing of diabetic wounds. Fibroblast growth factor 21 (FGF21) inhibits inflammation and promotes tissue regeneration, but it's limited by short half-life and poor stability. Poloxamer (P) hydrogel is a sustained drug delivery system. Therefore, this study aimed to investigate the role of macrophage dysfunction on the promotion of wound healing by rhFGF21-P hydrogel in type 2 diabetes mellitus (T2DM) murine models and murine peritoneal macrophages (MPMs) stimulated with high glucose and LPS (HG + LPS) for in vitro studies. P hydrogel sustained the release and enhanced the stability of rhFGF21. RhFGF21-P administration accelerated diabetic wound closure and reduced the levels of TNF-α, IL-6, MCP-1 and MIP-2 in diabetic mouse serum and skin tissues as well as in HG + LPS-stimulated MPMs. RhFGF21-P attenuated the fluorescence intensity of F4/80 and increased the level of autophagy in T2DM wound mice. RhFGF21 enhanced phagocytic capacity and the expression of LC3II protein in HG + LPS-stimulated MPMs, and the regulation of rhFGF21 in inflammatory cytokines and phagocytosis was reversed by autophagy inhibitors (3MA and CQ). In addition, rhFGF21 downregulated the levels of STING in vivo and in vitro. Furthermore, rhFGF21 increased the expression of LC3II protein, inhibited the mRNA levels of inflammatory cytokines (TNF-α and IL-6) and enhanced phagocytosis in HG + LPS-treated MPMs, but these effects were reversed by the STING agonist Vadimezan. These results demonstrated that rhFGF21-P promoted diabetic wound healing through inhibiting the expression of inflammatory cytokines and enhancing phagocytic function of macrophages via the modulation of STING-mediated autophagy. - Source: PubMed
Publication date: 2026/05/17
Li JianaQiu RuiyingYe ShashaLin JingjingWu JunyiWang YiRanChen JunZhao Yeli - End-stage renal disease (ESRD) is frequently accompanied by systemic inflammation and pulmonary dysfunction. Fibroblast growth factor-21 (FGF-21), an emerging metabolic and inflammatory biomarker, may be involved in these pathological processes. This study aimed to evaluate dynamic changes in FGF-21 and their association with inflammatory markers-including C-reactive protein (CRP) and interleukin-6 (IL-6)-as well as pulmonary function in ESRD patients receiving peritoneal dialysis (PD). - Source: PubMed
Publication date: 2026/05/15
Lin ChangdaChe LishuangZhang YunLi YuetingChen Jinhai - Esophageal squamous cell carcinoma (ESCC) is a highly prevalent malignancy worldwide. Curcumin is a well-known phytochemical with proven anticancer properties. However, it has poor bioavailability and is unstable. Therefore, the purpose of this study was to develop curcumin nanoparticles and explore the antitumour effects of curcumin and nano-curcumin in ESCC. Nano-curcumin was successfully prepared by the thin-film hydration method. The results of MTT assay, colony formation assay, and apoptosis assays demonstrated that both curcumin and nano-curcumin inhibited the proliferation of ESCC cells. Curcumin and nano-curcumin could regulate the expression of BAX, BCL2, and caspase-3 in ESCC cells. We found that curcumin and nano-curcumin could also induce reactive oxygen species production and decrease the mitochondrial membrane potential. The sequencing results indicated that curcumin and nano-curcumin inhibited ESCC proliferation through calcium signalling pathways in KYSE450 cells. Furthermore, curcumin and nano-curcumin increased calcium levels. RT-qPCR and Western blot data also demonstrated that both curcumin and nano-curcumin promote endoplasmic reticulum (ER) stress in ESCC cells. By establishing a xenograft tumour model of ESCC, curcumin and nano-curcumin inhibited tumour proliferation and induced apoptosis and ER stress, indicating that curcumin and nano-curcumin exerted antitumour effects in vivo. Therefore, our findings provide a potential lead compound for treating ESCC. - Source: PubMed
Publication date: 2026/05/13
Zhao LiyingLuo MengqiangQian ChunmeiLiu ChengWang YiyingChen MiaoxinCui WeiWang Xiaoyu