Ask about this productRelated genes to: ANXA1 protein
- Gene:
- ANXA1 NIH gene
- Name:
- annexin A1
- Previous symbol:
- ANX1, LPC1
- Synonyms:
- -
- Chromosome:
- 9q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: ANXA1 protein
Related articles to: ANXA1 protein
- Egg yolk oil (EYO) has been traditionally applied to treat skin fissures and burns. It has long been applied topically to promote wound healing and alleviate inflammation. Despite its extensive historical use and reported clinical benefits, the scientific basis and molecular mechanisms underlying its therapeutic effects, particularly in deep second-degree burn repair, remain insufficiently understood. - Source: PubMed
Publication date: 2026/05/05
Gao Xiao-FaLin Zi-BoWang JunWu Shi-JinLi HuanLi Fang-SenHan Si-QianXie Li-FengShao Hong-WeiLiu Song - Childhood obesity is tightly linked to dyslipidemia, chronic low-grade inflammation, and insulin resistance (IR). CD36 has been implicated in metabolic disease, yet its pediatric mechanisms remain unclear. This study aims to investigate the CD36/ANXA1/TLR4/NF-κB axis as a potential therapeutic target for lipid metabolism and IR in childhood obesity. - Source: PubMed
Publication date: 2026/05/04
Yao YiqingYang WeimingCheng FengMao Shunfeng - Heatstroke is a life-threatening condition characterised by severe inflammation and often linked to necroptosis, a form of programmed cell death mediated by receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like pseudokinase (MLKL). Annexin A1 (AnxA1) is known to play a role in resolving inflammation, but its effects on heatstroke remain unclear. This study investigates the role of AnxA1 in heatstroke and its potential mechanisms. - Source: PubMed
Publication date: 2026/05/04
Feng BoLi HuiPan Xiao DongZhang Wen YanLi Xin YuJiang Ya TingLiu Lin FengBhandari SuwasLuo JunWeng Hai XuChen JieDing Ya JunChen TingJin Hai XiaZhu Xin YiXin Xian MingGong Yu QiangJin Sheng WeiHao Yu - Annexin A1 (ANXA1) is a proresolving protein regulated by glucocorticoids, the standard care for severe and critical COVID-19 patients. As part of a larger project including hospitalized COVID-19 patients, this study aimed at evaluating ANXA1 and its FPR2 receptor in these patients, focusing on longitudinal profiles and comparison across disease severities and outcomes, and exploring their correlations with inflammation, endotheliitis and other proresolving mediators. Blood was collected in "severe" ( = 27), "critical" ( = 17) and "critical on veno-venous extracorporeal membrane oxygenation" ( = 17) COVID-19 patients at admission, days 3-4, 5-8, and weekly thereafter, and in controls ( = 23) at a single time point. We quantified ANXA1, resolvin D1, resolvin E1 (RvE1) and endocan by ELISA, cytokines and other endothelial markers by multiplex immunoassays, and FPR2 and Chemerin receptors by RT-qPCR. Most patients underwent a 10-day dexamethasone regimen. Admission ANXA1 and were significantly higher in all patient groups. Throughout hospitalization, ANXA1 increased mainly in "severe" patients and survivors, becoming higher at weeks 3 and 4 in survivors versus non-survivors. Variable cumulative dexamethasone doses did not differentially affect ANXA1 or . ANXA1 was associated with higher RvE1 during the dexamethasone effect period. Exploratory analyses showed that ANXA1 inversely correlated with RvE1 receptor and endotheliitis, whereas both ANXA1 and positively correlated with inflammation. In conclusion, ANXA1 may be involved in COVID-19 recovery processes, and its interplay with RvE1 may ameliorate hyperinflammation. - Source: PubMed
Publication date: 2026/03/28
Silva-Pereira CarolinaReina-Couto MartaPereira-Terra PatríciaTeixeira-Santos LuísaMartins SandraPinho DoraSoares Miguel LuzDias Cláudia CamilaSarmento AntónioTavares MargaridaGuimarães João TiagoPaiva José-ArturFraga SóniaAlbino-Teixeira AntónioRoncon-Albuquerque RobertoSousa Teresa - Heat stroke (HS) causes high mortality via multiple organ dysfunction syndrome, with intestinal barrier dysfunction as an early trigger of systemic inflammation. However, the roles of annexin A1 (ANXA1) in HS-induced intestinal barrier dysfunction remain unclear. Therefore, this study investigated the roles of ANXA1 in HS-induced intestinal barrier dysfunction through integrating single-cell transcriptomics and in vivo experiments. The single-cell RNA sequencing (scRNA-seq) data were used to analyze the cell subpopulation changes between healthy controls and HS patients, as well as between the inflammatory sites and non-inflammatory sites in inflammatory bowel disease. In vivo, the H&E staining, flow cytometry, ELISA, and Western blot were used to determine the pathological injuries, the proportion of neutrophils and monocytes, inflammatory cytokine levels, and related protein expression levels in the colon tissue. Immunofluorescence co-localization analysis was performed to detect the interaction between ANXA1 and immune cells. The scRNA-seq data showed that the proportion of neutrophil and CD14Mono subpopulations was increased in HS patients. Concurrently, the ANXA1 expression was significantly upregulated in multiple immune cell subpopulations, including the CD14Mono, CD16Mono, mDC, MDSC, and neutrophil subpopulations. Cell-cell communication analysis further demonstrated that the ANXA1-formyl peptide receptor 2 (FPR2) ligand-receptor pairs were the dominant mode of interaction during HS. Importantly, there was partial overlap between cell populations expressing ANXA1 and barrier genes. In addition, ANXA1 was positively associated with M2 monocyte phenotype in both inflammatory and non-inflammatory sites. After establishing the HS model, there were some alterations in the colon tissue, including the exacerbated pathological injuries, upregulated ANXA1 and FPR2 protein expression levels, downregulated ZO-1 and occludin protein expression levels, increased inflammatory cytokine levels, and activated TLR4/ERK/NF-κB pathway. Immunofluorescence co-localization analysis revealed that the mean density of ANXA1, CD14, and Ly6G in the colon tissue of HS mice was significantly elevated compared with the control group, and the co-localization of ANXA1 with CD14 and ANXA1 with Ly6G was enhanced. The treatment of Boc1 led to a dramatic reduction in ANXA1 mean density, a further increase in CD14 and Ly6G mean density, and a reduction in the co-localization of ANXA1 with CD14 and Ly6G. Apart from reversing the ANXA1 and FPR2 protein expression levels, inhibiting ANXA1 aggravated the damaging effects of HS on the colon tissue. In conclusion, ANXA1 protected against HS-induced intestinal barrier dysfunction by regulating neutrophil-monocyte interaction and inhibiting TLR4/ERK/NF-κB, with ANXA1-FPR2 as a key axis, which offers a novel target and strategy for the clinical treatment of HS-induced intestinal barrier dysfunction. - Source: PubMed
Publication date: 2026/04/30
Li JunChen XuemeiTong ZewenJin Yishun