Ask about this productRelated genes to: FGL2 antibody
- Gene:
- FGL2 NIH gene
- Name:
- fibrinogen like 2
- Previous symbol:
- -
- Synonyms:
- pT49, T49
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2016-02-03
Related products to: FGL2 antibody
Related articles to: FGL2 antibody
- The search for additional therapies against acute rejection is warranted. Alternatively activated macrophages (M2 macrophages) have immunomodulatory functions, and enhancement of their immunomodulatory capacity is a feasible complementary therapy. Fcγ receptor II b (FcγRIIb, CD32b), which is highly expressed by M2 macrophages, and its important ligand, fibrinogen-like protein 2 (Fgl2), are immunosuppressive molecules, and it is necessary to explore the potential of both to enhance the immunomodulatory capacity of M2 macrophages. - Source: PubMed
Publication date: 2026/06/05
Ji WenbinZhang BaotongZhang JianshengChen GuoshanWang WeiweiQi Feng - Fibrinogen-like protein 2 (FGL2) participates in inflammatory and immune regulation; however, its contribution to airway smooth muscle cell (ASMC) dysfunction remains poorly defined. This study investigated the role of FGL2 in platelet-derived growth factor-BB (PDGF-BB)-induced pathological responses in ASMCs and explored the underlying signaling mechanisms. - Source: PubMed
Publication date: 2026/05/12
Zhao BoChe Yanran - Diabetic nephropathy (DN) is a major cause of chronic kidney disease, and sensitive biomarkers of early tubular injury remain limited. Fibrinogen-like protein 2 (FGL2) has been implicated in inflammation and fibrosis, but its clinical significance and mechanistic role in DN are unclear. Serum FGL2 levels were measured in 105 patients with T2DM stratified by albuminuria and in 110 healthy controls, and its associations with metabolic parameters, renal injury, inflammation, and fibrosis were analyzed. , HK-2 cells were exposed to high glucose, and FGL2 was silenced using siRNA to assess effects on PI3K/Akt-FoxO1 signaling, cell viability, apoptosis, oxidative stress, and ECM remodeling. Pathway specificity was confirmed using a PI3K/Akt inhibitor. Serum FGL2 levels were higher in patients with T2DM than in controls and increased progressively with the severity of albuminuria. Circulating FGL2 positively correlated with glycemic indices, insulin resistance, lipid parameters, renal tubular injury markers (NGAL, KIM-1), inflammatory cytokines (TNF-α, IL-6), and fibrotic mediators (TGF-β1, CTGF). High glucose induced FGL2 expression in HK-2 cells in a dose-dependent manner. Silencing FGL2 enhanced Akt and FoxO1 phosphorylation, improved cell viability, reduced apoptosis, attenuated oxidative stress, restored antioxidant enzyme activity, and suppressed ECM-related gene and protein expression. These protective effects were reversed by PI3K/Akt inhibition. Serum FGL2 is elevated in patients with T2DM and correlates with the severity of renal injury, while mechanistically contributing to high glucose-induced tubular dysfunction the PI3K/Akt-FoxO1 signaling pathway. - Source: PubMed
Publication date: 2026/05/20
Lu Xiao GangJin HuiWang Ya PeiLi Hong BinCheng Yin Qin - Understanding the pathogenesis of amyloid- pathology in Alzheimer's Disease (AD) proves to be a challenge. In this work, we expand upon the application of network diffusion models (NDM) to study pathophysiological spread of amyloid- throughout white matter structural brain networks. We found that the NDM successfully recaptures subpopulation-level spatial patterns (Pearson's R = 0.45-0.48, P < 0.01) of amyloid- deposition in the Alzheimer's Disease Neuroimaging Cohort at a regional level, but with drawbacks in mechanism interpretability. We then moved to an extended NDM framework (eNDM), including a protein synthesis term to better reflect the role of amyloid- metabolism, as well as including regional vulnerability using spatial transcriptomics from the Allen Human Brain Atlas to modulate the region-level rate parameters of the synthesis term. The novel gene eNDMs exhibited significant performance increases in Pearson's correlation (Steiger's Z, P < 0.10) over baseline NDM performance in mild cognitive impairment and AD groups using APOE, SORL1, and FGL2 for gene modulation. The results were robust and replicable when testing on an external cohort of the Alzheimer's Disease Sequencing Project. The study thus demonstrates the importance of regional genetic vulnerability, in conjunction with network diffusion mechanisms, in improving the modelling and prediction of amyloid- pathophysiological spread. - Source: PubMed
Publication date: 2026/05/07
Xu Frederick HDuong-Tran DuyHuang HengSaykin Andrew JThompson Paul MDavatzikos ChristosZhao YizeShen Li - Sepsis-associated acute kidney injury (SA-AKI) is significantly associated with high morbidity and mortality rates. Emerging evidence has suggested that ferroptosis plays a key role in AKI. It has been also reported that irisin exerts anti-inflammatory, anti-oxidative and anti-apoptotic properties. However, its protective effect, particularly via regulating ferroptosis, in AKI remains unclear. Therefore, the present study aimed to investigate the potential of irisin to restrain ferroptosis and relieve SA-AKI via activating fibrinogen-like 2 (FGL2). For the in vivo experiments, a lipopolysaccharide (LPS)-induced AKI model was established in wildtype and FGL2 mice. The effects of irisin in vitro were assessed in LPS-induced HK-2 cells. The results demonstrated that irisin could alleviate AKI, and attenuate ferroptosis and mitochondrial dysfunction in LPS-induced mice. However, these effects were partly abolished in FGL2 mice. Additionally, the results revealed that irisin inhibited reactive oxygen species accumulation and malondialdehyde levels, while increasing superoxide dismutase activity and glutathione levels in HK2 cells. However, the protective effects of irisin on LPS-induced HK-2 cells were abrogated following FGL2 silencing. In conclusion, irisin could protect against SA-AKI via conferring resistance to ferroptosis through activating FGL2. These findings indicated that irisin could represent a potential therapeutic approach for the treatment of SA-AKI. - Source: PubMed
Publication date: 2026/05/13
Yin SupeiWang YinHuang DongliQuan ZhihuiTao Rui