Ask about this productRelated genes to: LCN2 protein
- Gene:
- LCN2 NIH gene
- Name:
- lipocalin 2
- Previous symbol:
- -
- Synonyms:
- NGAL, 24p3
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-29
- Date modifiied:
- 2016-10-05
Related products to: LCN2 protein
Related articles to: LCN2 protein
- Chronic kidney disease (CKD) is a major global health burden characterized by progressive loss of renal function, persistent inflammation, and tubular epithelial injury, yet reproducible diagnostic biomarkers that also have functional relevance remain insufficiently defined. Here, we integrated multiple independent CKD transcriptomic cohorts from GEO (GSE32591 and GSE66494 as training datasets, with GSE180394 as an external validation dataset) using rigorous batch-effect correction and differential expression analysis to identify consistently dysregulated genes across platforms. Shared CKD-upregulated genes were predominantly enriched in immune and inflammatory biological processes, and module-level analyses prioritized a core set of hub genes showing stable activation across cohorts. Based on these hubs, we constructed a composite diagnostic gene signature using a standardized Z-score-based scoring approach, which demonstrated a robust discriminative performance in both training and external validation cohorts. Among candidate genes ranked by diagnostic performance, IFIT2 emerged as a reproducibly upregulated marker with strong diagnostic utility. Mechanistically, IFIT2 was inducible in human renal tubular epithelial cells (HK-2 and primary RPTEC) under CKD-relevant inflammatory (IFN-) and profibrotic (TGF-1) stimulation. Importantly, shRNA-mediated IFIT2 knockdown mitigated IFN--induced reductions in cell viability, decreased apoptosis, and attenuated the induction of tubular injury markers (KIM1 and LCN2) and inflammatory mediators (IL6 and CXCL10). Together, these results support IFIT2 as a promising candidate biomarker linking inflammation to tubular injury in CKD, providing a translational rationale for further biomarker-guided stratification and therapeutic targeting in future studies. - Source: PubMed
Publication date: 2026/05/16
Zhang XiaolingChen XueyanYang YaZhang Yiyuan - Acute kidney injury (AKI) is a serious entity characterized by sudden impairment of renal function in hospitalized patients, particularly in the intensive care unit, resulting in high morbidity and mortality. Current diagnostic methods based on changes in serum creatinine (sCr) and urine output are prone to many confounding variables. The aim of this study is to investigate the role of specific biomarkers, namely NGAL, Cystatin C, IL-18, and KIM-1, in the diagnosis of AKI. In this literature review, a thorough search of the PubMed, Scopus and Google Scholar databases was conducted to investigate the early diagnostic potential of NGAL, Cystatin C, IL-18, and KIM-1 in AKI patients. Neutrophil Gelatinase-Associated Lipocalin (NGAL), both serum and urinary, was discovered to rise shortly after AKI onset, several hours before sCr elevation, differentiating AKI from chronic kidney disease and prerenal azotemia. Cystatin C (CysC), a protein constantly produced and filtered, was identified as a reliable marker for AKI, although its high cost prohibits its use. Interleukin-18 (IL-18), a pro-inflammatory cytokine, demonstrated potential, particularly in critically ill and post-cardiovascular surgery patients, although results on its predictive ability were inconsistent. Kidney Injury Molecule-1 (KIM-1), a protein released into urine after proximal tubular injury, demonstrated high sensitivity and specificity shortly after AKI onset, while it has been associated with a number of kidney diseases. Novel biomarkers (NGAL, CysC, IL-18, and KIM-1) provide a faster and more accurate diagnosis of AKI than traditional methods in various clinical settings. Additional research is required to fully incorporate these promising molecules into everyday clinical practice. - Source: PubMed
Publication date: 2026/04/30
Gerasopoulos GeorgiosKapellakis-Malliaras AndreasPavlou Achilleia-Maria - Sialadenitis represents an intricate inflammatory condition affecting the salivary glands, marked by tissue damage, inflammation, and compromised secretory function, though targeted therapeutic approaches with proven efficacy continue to be scarce. Lipocalin-2 (Lcn2), a versatile protein that participates in inflammation and apoptosis regulation, has been associated with numerous inflammatory conditions. The present research examined the protective function of Lcn2 in sialadenitis, with particular focus on its anti-inflammatory and anti-apoptotic mechanisms as well as its latent capacity as a therapeutic target. Lcn2-associated alterations in salivary gland tissues and cells were evaluated through assessments of inflammatory injury, apoptotic markers (caspase-3, Bax, Bcl2), and functional molecules critical for glandular secretion (AQP5, MUC1, α-amylase) using human samples, LPS-induced murine models, RNA sequencing, immunohistochemistry, Western blotting, and siRNA-mediated Lcn2 knockdown. To further assess the functional role of Lcn2, mice were administered adeno-associated virus 2 (AAV2) to suppress Lcn2 expression during LPS-induced sialadenitis. LPS treatment markedly induced glandular damage, inflammation, and apoptosis, accompanied by robust upregulation of Lcn2. Lcn2 co-localized with caspase-3 in epithelial cells, and its suppression aggravated apoptosis and inflammation, whereas AAV2-mediated Lcn2 knockdown exacerbated tissue injury and disrupted secretion-related protein expression. Mechanistically, Lcn2 knockdown further enhanced LPS-induced phosphorylation of NF-κB p65, JNK, and p38. Inhibition of NF-κB with BAY11-7082 abolished the excessive inflammatory response, while inhibition of JNK with SP600125 attenuated the pro-apoptotic effect of Lcn2 silencing. Moreover, molecular docking and co-immunoprecipitation confirmed a direct physical interaction between Lcn2 and Bcl2. Conversely, Lcn2 overexpression alleviated these deleterious effects by modulating apoptotic and inflammatory mediators. Collectively, these findings demonstrate that Lcn2 confers protection against salivary gland injury in sialadenitis by regulating apoptosis and inflammation, at least partially via directly binding to Bcl2 and suppressing NF-κB and JNK/p38 MAPK signaling pathways, highlighting Lcn2 as one prospective therapeutic target for alleviating salivary gland dysfunction and inflammation. - Source: PubMed
Publication date: 2026/05/16
Feng GuijuanLi JingHuang LiliXia YunfeiYang JunlingCheng ChunGu Zhifeng - Essential thrombocythemia (ET) is a myeloproliferative disorder characterized as excessive platelet production. Early and accurate diagnosis is critical to manage the disease and prevent progression to serious myeloid neoplasms like myelofibrosis or acute myeloid leukemia, though definitive diagnosis remains challenging. - Source: PubMed
Publication date: 2026/04/29
Li YeqiongChen XiangguoGuo YingSha RongrongHao HuichengZhang JinSong HonghongWei YupingYe Xiupeng - Prostate cancer (PCa) is a hormone-dependent tumor and one of the most prevalent cancers in men worldwide. PCa progression is influenced by its interaction with the surrounding tumor microenvironment, highlighting the role of periprostatic adipose tissue (PPAT), which modulates PCa behavior through the secretion of bioactive molecules (e.g., adipokines). However, the influence of this complex cell communication, particularly under altered metabolic conditions, remains to be fully elucidated. - Source: PubMed
Publication date: 2026/05/14
Pérez-Gómez Jesús MPrats-Escribano AntonioGil-Duque IgnacioArroyo-Millán LauraHuertas-Cabrera HugoNúñez-Santos Miguel ALópez-Ruiz Daniel JMata-Ordoñez FernandoGonzález-Serrano TeresaOrtea IgnacioPorcel-Pastrana FranciscoÁlvarez-Benito MarinaPlanque MélanieCarrasco-Valiente JuliaGómez-Gómez EnriqueGuzmán-Ruiz RocíoFuentes-Fayos Antonio CFendt Sarah-MariaGahete Manuel DSarmento-Cabral AndréMalagón María Del MarLuque Raúl M