Ask about this productRelated genes to: FLT4 antibody
- Gene:
- FLT4 NIH gene
- Name:
- fms related tyrosine kinase 4
- Previous symbol:
- -
- Synonyms:
- VEGFR3, PCL
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-10-25
- Date modifiied:
- 2016-10-05
Related products to: FLT4 antibody
Related articles to: FLT4 antibody
- Implant-related osteomyelitis presents a significant clinical challenge, characterized by bacterial invasion, aggressive inflammation, and impaired osteogenesis. Zn-based implants are biodegradable and bacteriostatic, showing great potential for bone repair, however, the excessive release of Zn ions induces cytotoxicity and impacts early bone formation. To overcome this limitation, biomimetic selenium-doped Ca(PO)SiO nanoleaves (Se-CPS) were fabricated on Zn-1Ca (ZN) substrate. Se-CPS not only moderates the degradation of ZN, maintaining Zn release within a biocompatible range, but also sustainably supplies therapeutic ions (Se, Ca, Si, P) and establishes an alkaline microenvironment. When bacteria invade, the combined action of Zn ions and alkalinity eliminates 75-88% of bacteria by generating abundant intracellular reactive oxygen species (ROS), and concurrently, macrophages clear residual bacteria through enhanced xenophagy, a process driven by regulating the key autophagy-related genes (LC3-I/LC3-II, p62, Beclin 1, FLT4 and ATG5). Following bacterial eradication, antioxidative function of Se-CPS-mediated by the upregulation of selenoprotein genes (GPx1, GPx3, GPx4, TrxR1, SEPSH1, DIO1) restores cell viability and promotes the polarization of macrophages from the pro-inflammatory M1 to the pro-healing M2 phenotype. The combined antibacterial, immunomodulating, and osteogenic effects of Se-CPS were further validated in an osteomyelitis model, demonstrating enhanced osteointegration. This work presents an effective surface engineering strategy for Zn-based implants, enabling simultaneous infection control, inflammation modulation, and accelerated biointegration in an osteomyelitis microenvironment. - Source: PubMed
Publication date: 2026/04/23
Mao MengtingChen JunZhao LinLi QinyanLiu XinyueLiu YanZhang Lan - Atherosclerosis, the cholesterol-driven inflammatory process underlying cardiovascular disease (CVD), remains the leading cause of death in high-income countries despite major advances in risk factor management. This underscores the urgent need for therapies that directly target plaque development and progression. Recent evidence has uncovered an important role for lymphatic vessels in cardiovascular health: by facilitating reverse cholesterol transport, lymphatics help clear excess cholesterol from arterial walls and influence atherosclerosis from its earliest stages to advanced disease. Enhancing lymphatic pumping before atherogenesis limits plaque formation, while restoring lymphatic function in established atherosclerosis reduces lesion size and promotes stabilization. CVD risk rises sharply after menopause, and lymphedema studies suggest that women experience a more pronounced age-related decline in lymphatic pumping than men, pointing to a potential link with hormonal fluctuations. Hormonal changes throughout life-whether due to aging, therapeutic interventions, or personal choice-are key determinants of CVD vulnerability. Yet, how these changes affect lymphatic transport in individuals predisposed to CVD remains unexplored. - Source: PubMed
Publication date: 2026/03/11
Mesples MonaLacroix ÉlizabethTessier NolwennFarhat MayaMilasan AndreeaBabran SaraFernandez CristinaLatendresse TallyBenoit JustinLong ValérieGuillemette JulieEl Khakani SamiAlikashani AzadehLeblanc Charles-AlexandreHiggins Marie-ÈveDurocher-Granger VanessaFiset CélineMartel Catherine - In the brain, endothelial cell (EC) subtypes characterized by blood-brain barrier (BBB) properties or fenestrated pores form essential brain-blood interfaces and exhibit markedly distinct permeability. The choroid plexus (CP) establishes fenestrated vasculature lacking the BBB to efficiently regulate cerebrospinal fluid balance, yet its developmental origins and mechanisms remain poorly defined. Using single-cell-resolution fate mapping in zebrafish, we identify here two venous sources that give rise to the hindbrain myelencephalic CP (mCP) vasculature. RNAscope and BAC transgenic analyses reveal highly abundant and persistent expression of the venous marker in these EC lineages, supporting their identities. Unexpectedly, we find that these venous origins of the mCP vasculature also contribute ECs to diverse cranial vessels, including those that maintain low expression and later acquire BBB characteristics. Functionally, null and cytoplasmic-domain-deletion mutants exacerbate mCP vascularization defects when combined with signaling deficiency, without disrupting neighboring BBB-type vessels. Pharmacological data support this corequirement of Flt4 and Vegfr2 signaling in mCP vascularization and further suggest that the PI3K and ERK pathways are necessary for this process. Together, these findings reveal embryonic venous lineages and molecular pathways required for hindbrain CP vascularization and imply that Flt4 signaling contributes to the angiogenic separation of CP- and BBB-associated capillaries originating from shared embryonic domains. - Source: PubMed
Publication date: 2026/04/15
Lee Nathanael JBozdag Fatma ZLeong Jun XiongParab SwetaLam Amanda EThakur VaniMatsuoka Ryota L - Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, classically characterized by right ventricular outflow tract obstruction, ventricular septal defect, overriding aorta, and right ventricular hypertrophy. Recent advances in molecular and genomic research indicate that TOF is part of a phenotypic continuum encompassing Trilogy, Tetralogy, and Pentalogy of Fallot, in which the variability of anatomical presentation reflects shared genetic and epigenetic mechanisms with highly variable penetrance and expressivity. Variants in , , , , and highlight key pathways in conotruncal development and endothelial-mesenchymal transition, yet these well-known genes explain only a fraction of the genetic landscape. Emerging studies have identified additional candidate genes and networks involved in cardiac morphogenesis, including transcriptional regulators, signaling mediators, chromatin-remodeling factors, and splicing-associated genes such as PUF60 and DVL3. Epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNA expression, further modulate phenotypic expressivity and contribute to variability along the Trilogy-Tetralogy-Pentalogy spectrum. This review integrates current genomic and clinical evidence to provide a comprehensive overview of the molecular architecture of Fallot-type conotruncal malformations, emphasizing the interplay between genetic and epigenetic mechanisms, genotype-phenotype correlations, and implications for diagnosis, risk stratification, counseling, and personalized management in the era of precision cardiology. - Source: PubMed
Publication date: 2026/01/31
Gagliardi Maria FeliciaMicaglio EmanueleMicheletti AngeloBenedetti SaraNegura Diana GabrielaBevilacqua FrancescaGuglielmi GiuliaPasqualin GiuliaGiamberti AlessandroChessa Massimo - Brain meninges contain lymphatic vessels that play roles in clearance of extracellular solute in the central nervous system. But, whether and how the system is involved in acute stroke remains to be fully explored. Here, we show the VEGF-C-Flt4 pathway involvement in brain swelling in acute phase of ischemic stroke in rats. We first confirmed that a prototypical lymphatic mediator VEGF-C was upregulated in brain endothelium and secreted into CSF. Concomitantly, VEGF-C receptor Flt4 was increased in the meninges but not in peri-infarct cortex. Next, we isolated lymphatic endothelial cells from rat meninges using LYVE-1 antibody-conjugated magnetic beads. An in vitro standard matrigel assay confirmed that isolated LYVE1 + cells increased ring-like structures by treatment with VEGF-C or conditioned media from injured brain endothelium subjected to oxygen-glucose deprivation, whereas immunodepletion of VEGF-C from endothelial media decreased the effect. Finally, blocking Flt4 tyrosine kinase in vivo suppressed the acute increase of lymphatic endothelial cells accompanied by reduction of brain swelling. Collectively, the proof-of-concept study suggests that the VEGF-C-Flt4 signaling pathway contributes to brain swelling during the acute phase of ischemic stroke by activating meningeal lymphatic endothelial cells. Targeting this pathway may offer a new approach to mitigate stroke-induced inflammation and edema. - Source: PubMed
Publication date: 2026/02/12
Patil Rohan MaheshBack Dong BinHamanaka GenDesai RakhiHayakawa AyumiChan Su JingAhn Bum JuPignataro GiuseppeHayakawa KazuhideEsposito Elga