Ask about this productRelated genes to: VEGFC protein (Rat) (152s)
- Gene:
- VEGFC NIH gene
- Name:
- vascular endothelial growth factor C
- Previous symbol:
- -
- Synonyms:
- VRP
- Chromosome:
- 4q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2015-08-26
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- Oral Squamous Cell Carcinoma (OSCC) is a common epithelial malignancy with a persistently poor prognosis, largely influenced by regional lymph node status. Current treatment of OSCC relies on the TNM staging system, which does not include the molecular characteristics of the neoplasm. This study aimed to evaluate lymph node morphologic patterns and molecular markers of lymphangiogenesis to support biologically informed pathologic risk stratification. - Source: PubMed
Publication date: 2026/07/29
Tandon AnkitaSandhya KumariSingh Shashi BhushanSanga Aradhana - The characteristics of diabetic vascular complications are impaired angiogenesis, which leads to hindlimb ischemia. Although astragaloside IV (AS-IV) can promote angiogenesis, its poor targeting to endothelial progenitor cells (EPCs) limits its therapeutic effect. Here, we developed liposomes modified with iRGD to load AS-IV (Lp-iRGD@AS-IV) to enhance its delivery and explored its mechanism. Lp-iRGD@AS-IV and fluorescently labeled liposomes were prepared, and their phenotypic characteristics were detected. The study results showed that the uptake efficiency of Lp-iRGD@AS-IV by EPCs was higher than that of Lp@AS-IV. In a diabetic mouse hindlimb ischemia model induced by streptozotocin, Lp@AS-IV and Lp-iRGD@AS-IV improved cell damage, increased capillary density, and reduced reactive oxygen species accumulation. However, the therapeutic effect of Lp-iRGD@AS-IV was more significant than that of Lp@AS-IV. Lp-iRGD@AS-IV attenuated high glucose-induced inhibitory effect on cell viability, migration, and invasion capability of EPCs. Additionally, we analyzed the regulatory effects of the Hippo-YAP/TAZ signaling pathway in diabetic vascular complications. AS-IV increased the expression of vascular growth factors (VEGFa, VEGFb, VEGFc, FGF, and Ang-1), eNOS, and osteopontin, and enhanced glucose-lipid metabolism, via activating the upstream Hippo signaling pathway while inactivating the downstream YAP/TAZ activity. In conclusion, Lp-iRGD@AS-IV significantly enhanced the delivery of AS-IV to EPCs and improved hindlimb ischemia in diabetic mice. AS-IV can restore diabetes-associated impaired angiogenesis through the Hippo-YAP/TAZ pathway. Lp-iRGD@AS-IV may be a targeted therapy for diabetic vascular complications. - Source: PubMed
Publication date: 2026/07/24
Zeng ChuruoLi QinxiaGuo DongweiXiong WuZou XiaolingLi WeiBin JieWang XiupingZhang ZihaoXue BingqianHu RuoweiZhang Xi - Meningeal (dural) lymphatics are essential for cerebrospinal fluid (CSF) clearance to cervical lymph nodes, yet the precise pathway is incompletely understood. Using a multifaceted approach in mice, we examined tracer dynamics and the CSF outflow pathway from the subarachnoid space (SAS) to the nasal mucosa and identified a discrete arachnoid region surrounding the olfactory bulbs with abundant fenestrations. Similar arachnoid fenestrations were found in cynomolgus monkeys. Fluorescent tracers in the SAS passed through arachnoid fenestrations into dural lymphatics, which traversed the cribriform plate foramina, joined the nasal lymphatics, and drained to the cervical lymph nodes. In aged mice, the known reduction in CSF outflow was accompanied by lymphatic atrophy in the olfactory dura and nasal mucosa and by fewer arachnoid fenestrations and smaller cribriform plate foramina. Importantly, the lymphatics and CSF clearance were restored to normal by intranasal delivery of vascular endothelial growth factor-C (VEGF-C), thereby documenting the reversibility of the aging-related impairment in CSF clearance. - Source: PubMed
Publication date: 2026/07/21
Hong Seon PyoJin CheolhwaYang Myung JinJin HokyungYoon Jin-HuiChoi Du RiJung JunhoYuk Chae MinAntila SalliSeo Su JinAdmasu Leul ASeo JincheolLim Kyung SeobChung Won-SukAlitalo KariMcDonald Donald MKoh Gou Young - Diabetic cardiomyopathy (DCM) is characterized by microvascular dysfunction. While vascular endothelial cells (ECs) have been widely studied, the role of cardiac lymphatic ECs (LECs) in DCM remains unknown. - Source: PubMed
Publication date: 2026/07/16
Yan YufengWang XunuoZhu CongfeiJiang ZihaoWang JingHe JunjieXu LeiZhou XiaobinGe QingHu ZuoyingZuo Guangfeng - Lymphoma can seriously affect the quality of life of patients. Both homoharringtonine (HHT) and tanshinone IIA (Tan IIA) have shown robust anti-proliferation and apoptosis-inducing effects in lymphoma cells. However, it is unclear whether they can be used in combination to treat acute myeloid leukemia and lymphoma. Cell Counting Kit-8 (CCK-8) was employed to measure cell viability, the 5-Ethynyl-20-deoxyuridine assay (EdU) was used to quantify cell proliferation, and the transwell migration assay was used to assess cell migration in U937 and Raji cells. Additionally, transmission electron microscopy and nanoparticle tracking analysis assays were used to observe and identify exosomal structure, respectively. Combined HHT and Tan IIA treatment synergistically inhibited the viability and proliferation of U937 and Raji cells, induced apoptosis, and reduced vascular endothelial growth factor (VEGF) levels in these cells. Additionally, VEGFA and VEGFC levels were significantly reduced in exosomes derived from Raji cells that had been treated with HHT and Tan IIA (Exo). Moreover, absorption of Exo significantly inhibited the viability, proliferation, and migration of human umbilical vein endothelial cells by downregulating the expression of serine/threonine kinase 1 (Akt), matrix metalloproteinase-2 (MMP2) and MMP9. Exo suppressed the tumor microenvironment. HHT and Tan IIA combined therapy synergistically suppressed lymphoma progression by downregulating the Akt/MMP signaling pathway, suggesting their use in treating lymphomas. Clinical trial number: Not applicable. - Source: PubMed
Publication date: 2026/07/10
Zhang YanpingYin JianLiu RuiMiu JiyuLiu ZeshiZhu JianhongHe Aili