Ask about this productRelated genes to: LRG1 protein
- Gene:
- LRG1 NIH gene
- Name:
- leucine rich alpha-2-glycoprotein 1
- Previous symbol:
- -
- Synonyms:
- LRG
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-12
- Date modifiied:
- 2016-06-06
Related products to: LRG1 protein
Related articles to: LRG1 protein
- As the most common microvascular complication of diabetes, diabetic retinopathy (DR) has become a leading cause of blindness among the global diabetic population. The pathogenesis of DR is not yet fully understood, and current clinical treatment options are limited and have suboptimal efficacy. A detailed investigation of the intercellular communication mechanisms during the progression of DR is of paramount importance. In this study, we first synthesized findings from various studies on classical pathways, including VEGF signaling, oxidative stress, inflammatory cascades, the polyol pathway, PKC signaling, and the Wnt/β-catenin pathway, with a focus on elucidating the cell-type specificity of each pathway and the interactions among them. Subsequently, we explored emerging mechanisms identified in recent years, such as the ethanolamine pathway, ANGPTL4, Lrg1, and Norrin-FZD4, to expand our understanding of the pathogenesis of DR. Through a systematic investigation of multiple pathways, we propose that the progression of DR is not driven by the effect of a single pathway but rather results from the dynamic interplay among these signaling networks. Additionally, we described recent advances in the clinical translation of related pathways, including multitarget therapeutic strategies and precision interventions mediated by pathway-specific biomarkers. This review aims to provide a comprehensive and integrative perspective on the mechanisms underlying DR, thereby establishing a theoretical foundation for experimental research and clinical translation. - Source: PubMed
Publication date: 2026/04/13
Wu ShenhaoGao Jing - Luminal breast cancer has a high incidence and significant heterogeneity. Exosomes, as key mediators of intercellular communication, are involved in the tumor process, but the related genes in Luminal breast cancer regarding prognosis and mechanism remain unclear. - Source: PubMed
Publication date: 2026/04/13
Huang JianTang XiulingSu QiyuanFang DalangWang JinLuo Zhizhai - The liver undergoes active remodeling by the primary tumor prior to metastatic spread. However, the mechanisms by which hepatocytes dictate the liver-specific tropism of tumors remain elusive. Here, we identify hepatocyte-derived leucine-rich alpha-2-glycoprotein 1 (LRG1) as a key mediator of liver premetastatic niche (PMN) formation. Clinically, elevated serum LRG1 levels are correlated with an increased risk of liver metastasis in patients and multiple mouse models. Mechanistically, LRG1 remodels the hepatic microenvironment by driving immunosuppressive neutrophil accumulation, impairing the function of effector T cells and dendritic cells, and enhancing angiogenesis in the liver, thereby fostering a prometastatic landscape. Hepatocyte-specific ablation of LRG1 dampens premetastatic niche formation and significantly reduces the metastatic burden in vivo. Hepatic LRG1 induced by tumor-associated inflammation via IL-6/STAT3 signaling promotes liver metastasis through the formation of TGFBR/PI3K/AKT axis-driven neutrophil extracellular traps (NETs). Importantly, therapeutic blockade of LRG1 not only suppressed liver metastasis but also reprogrammed the hepatic niche toward an immune-activated state, sensitizing tumors to anti-PD-1 therapy. Collectively, our findings reveal a hepatocyte-LRG1 axis that drives liver premetastatic niche remodeling and highlight LRG1 as a promising target for the prevention and treatment of liver metastasis. - Source: PubMed
Publication date: 2026/04/10
Long GuojieCheng BingJiang YueLiu QiufengHuang XiaomingNiu ZhitongXiao QianQian XiangjunWei ChaoyinChen JinxinWeng YingzhenZheng ZheyuLuo DandongMa TaoSu TingTang QiongweiWang PanpanChen YufengTan JingZhang RonghuaYu QiangPan WeidongWang Wenyu - Sepsis remains a leading cause of pediatric morbidity and mortality, yet its molecular underpinnings are poorly understood. Here, we performed mass spectrometry-based plasma proteomics and cytokine profiling in pediatric sepsis patients at the acute phase (AP) and recovery phase (RP), alongside preoperative surgical controls. In AP vs. control, we identified 41 differentially abundant (DA) proteins, including acute-phase reactants and complement factors, with persistent but attenuated expression in RP. Pathway analysis revealed sustained enrichment in inflammatory and complement activation processes during both AP and RP, with partial restoration of immune surveillance and vascular homeostasis in recovery. Machine learning highlighted complement components (C9, C1R) and LRG1 as candidate AP biomarkers, and S100A9 as an RP-associated marker. Comparative analysis with adult sepsis proteomes uncovered age-specific complement activation patterns: adults displayed higher classical pathway activity, whereas pediatric patients exhibited enhanced alternative pathway activity. Cytokine profiling confirmed sustained immune activation and endothelial perturbation across sepsis phases. We also compared the sepsis cohort with the sterile inflammation (SI) cohort, which revealed distinct adaptive immune enrichment in sepsis while innate immune predominance in SI, enabling the identification of potential sepsis-specific protein signatures. Together, these findings delineate the dynamic immune and vascular proteomic landscape of pediatric sepsis, reveal biomarkers distinguishing sepsis from sterile inflammation, and highlight age-related complement pathway differences with potential therapeutic implications. ClinicalTrials.gov: NCT04103268, NCT04299828. - Source: PubMed
Publication date: 2026/03/09
Alhamdan FahdSin Yi-ChengMalm ErikVan Pelt HannaKim SamuelHiggins LeeAnnChen YueYuki Koichi - Esophageal squamous cell carcinoma (ESCC) remains a lethal malignancy with a poor 5-year survival rate of approximately 20%, necessitating the identification of novel therapeutic targets. Here, we show that KDM4A is significantly upregulated in esophageal squamous cell carcinoma (ESCC) and its high expression correlates with poor prognosis. Functional assays demonstrated that KDM4A promotes ESCC cell proliferation, migration, invasion, and tumor growth in vitro and in vivo. Mechanistically, KDM4A demethylates H3K9me3 at the LRG1 promoter, thereby enhancing LRG1 transcription and activating the TGF-β pathway to drive epithelial-mesenchymal transition (EMT) and cancer stemness. Knockdown of KDM4A or LRG1 suppresses these oncogenic phenotypes, while LRG1 overexpression rescues KDM4A deficiency-induced impairments. Clinically, KDM4A and LRG1 are co-overexpressed in ESCC tissues and associated with advanced tumor stage and shorter overall survival. These findings identify the KDM4A-LRG1-TGF-β axis as a critical driver of ESCC progression and a potential therapeutic target. - Source: PubMed
Publication date: 2026/03/11
Han YuetingWang HuiyaGuo YaoyangZhang HongdianWen XinyiZhang MiaoGao ZhanhuaHao JieQiu MinghanRen LiHu DongzhiBa YiSun BeiZhang Haiyang