FGL

FGL-1 is a liver-derived secretory protein initially identified as a mitogenic factor in hepatocyte proliferation and liver regeneration.; Circulating FGL-1 levels are associated with obesity, insulin resistance, MASLD, and type 2 diabetes mellitus.; FGL-1 may contribute to metabolic dysfunction by impairing insulin signaling and promoting hepatic lipid accumulation, but its precise molecular targets are incompletely defined.; FGL-1 is a major ligand of LAG-3, implicating it in immune modulation and tumor progression, particularly in hepatocellular carcinoma, and may act as a context-dependent mediator rather than a purely pathogenic factor.

FGL-1 is a potent factor for interorgan communication between the liver and immune system in primary Sjögren disease.; Liver FGL-1 production is induced by interleukin-6 from CD4+ T cells.; Fgl1-deficient mice show earlier onset of autoimmune lesions compared to wild-type mice.; FGL-1 levels are significantly elevated in patients with primary Sjögren disease and correlate with serum IL-6 levels.

Comparable overall survival across chemotherapy, chemoimmunotherapy, and immunotherapy regimens without unexpected adverse events.; Genomic analysis reveals NSCLC-like (KEAP1, KRAS, STK11) and SCLC-like (RB1, TP53) LCNEC subtypes, with 80% aligning with SCLC transcriptional profiles.; Elevated FGL-1 and SPINK1 expression in NSCLC-like LCNECs, and higher DLL3 levels in SCLC-like LCNECs.; Fewer tumor-infiltrating lymphocytes in LCNECs compared to other lung cancers.

GL and FGL supplementation reduced fasting blood glucose levels and enhanced muscle strength and skeletal muscle cross-sectional area in T2DM mice.; Both GL and FGL ameliorated ubiquitin-proteasome system (UPS)-related pathways, while only FGL attenuated skeletal muscle inflammation and apoptosis.; FGL, administered at half the dose of GL, demonstrated greater efficacy in regulating molecular markers, including improved mTOR-autophagy pathway.; Bioconversion of guava leaf with L. plantarum produced unique metabolites (e.g., hydroxyl-isocaproic acid) and may offer additive or synergistic anti-diabetic and muscle-protective effects.

Liver FGL-1 mRNA was increased in AH versus healthy controls, whereas plasma FGL-1 was unchanged; Liver LAG-3 mRNA was reduced in AH, while plasma sLAG-3 and LAG-3+CD8+ T cell frequency were similar to healthy controls; Lowest plasma FGL-1 and lowest LAG-3+CD8+ T cell frequency at diagnosis were associated with highest disease severity and mortality; The data suggest an impaired FGL-1/LAG-3 axis may be involved in the pathogenesis and course of AH

G-Rb3-FGL co-treatment improved heart function better than G-Rb3 treatment alone in MI mice models; G-Rb3-FGL co-treatment upregulated fatty acid oxidation (FAO) and suppressed oxidative stress in heart tissues of MI mice; The synergistic effects of G-Rb3-FGL on FAO, oxidation, and inflammation were abolished by RXR inhibitor HX531 in the H9C2 cell model; G-Rb3 and FGL protected cardiomyocytes by promoting FAO, inhibiting oxidative stress, and suppressing inflammation through the RXR-Nrf2 signaling pathway

Major CAF types exhibit three activation states with distinct interactions and prognostic relevance for immunotherapy.; Minor CAF components can originate from other TME components such as endothelia and macrophages.; Endothelial-to-mesenchymal transition CAFs are ubiquitously present and may interact with SPP1+ tumor-associated macrophages, impacting survival.

No significant difference in LAG-3 expression on peripheral CD3+ T cells between normal pregnancy and early-onset preeclampsia; Significantly decreased LAG-3 expression on peripheral CD4+ and CD8+ T cells in early-onset preeclampsia compared to normal pregnancy; LAG-3 expression was higher on decidual T cells than peripheral T cells in all pregnancies; Plasma FGL-1 levels were significantly elevated in early-onset preeclampsia compared with normal pregnancy

What is FGL?

**Mechanism of Action** FGL (FG Loop peptide) is a synthetic peptide derived from the neural cell adhesion molecule (NCAM) that mimics the FG loop region of NCAM’s fibronectin type III domain. It selectively binds to and activates fibroblast growth factor receptor 1 (FGFR1), initiating downstream signaling cascades suc

How does FGL work?

NCAM-derived FG-loop peptide that activates FGFR1 to enhance synaptic plasticity and memory in animal models.

What is the research status of FGL?

FGL is currently classified as preclinical, with 263 research references on record. This is for research purposes only and is not medical advice.