Human VEGF-D Protein
- Known as:
- Human VEGF-D Protein
- Catalog number:
- VED-H5228
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human VEGF- Protein
Related genes to: Human VEGF-D Protein
- Gene:
- FLT1 NIH gene
- Name:
- fms related tyrosine kinase 1
- Previous symbol:
- FLT
- Synonyms:
- VEGFR1
- Chromosome:
- 13q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
- 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
- Gene:
- KDR NIH gene
- Name:
- kinase insert domain receptor
- Previous symbol:
- -
- Synonyms:
- FLK1, VEGFR, VEGFR2, CD309
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2019-04-23
- Gene:
- NRP1 NIH gene
- Name:
- neuropilin 1
- Previous symbol:
- -
- Synonyms:
- NRP, VEGF165R, CD304
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2016-10-05
- Gene:
- NRP2 NIH gene
- Name:
- neuropilin 2
- Previous symbol:
- -
- Synonyms:
- VEGF165R2
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2015-09-01
Related products to: Human VEGF-D Protein
Related articles to: Human VEGF-D Protein
- In endurance athletes, cardiovascular oxygen delivery is the primary limitation to performance. While the focus of athletes and regulatory bodies has been on hemoglobin and red blood cells, the increased oxygen-delivering capacity resulting from training is also a consequence of the expanded blood volume, which requires vascular adaptation. Angiogenesis-the formation of new blood vessels from pre-existing ones-is an understudied area in exercise physiology due to the need for invasive procedures. Among the vascular endothelial growth factors, VEGF-A and VEGF-D are the most potent angiogenic inducers and thus candidates for doping purposes. VEGF expression can be stimulated by several external factors, of which oxygen deprivation and its mimics are the most significant in the context of doping. A controlled overexpression of VEGF-A or VEGF-D, and the resulting blood vessel formation, could directly increase vascular space and indirectly increase blood volume and athletic ability. A master regulatory gene such as HIF-1α would be a preferred target over any single growth factor, as it would affect red blood cell production and vascular expansion synchronously. Currently available compounds may already be misused, with potential unintended consequences, including the aggravation of inflammatory diseases or tumor progression. Due to the ease of implementation and difficulty of detection, angiogenic doping and possible detection strategies deserve to be studied further. - Source: PubMed
Publication date: 2026/05/21
Lehto SofieSima SetarehKünnapuu JaanaIljukov SergeiJeltsch Michael - Lipedema is a chronic adipose tissue disorder characterized by disproportionate fat accumulation, pain, microvascular dysfunction, and low-grade inflammation. Although low-carbohydrate, high-fat (LCHF) dietary approaches are increasingly used in clinical practice, their longer-term associations with vascular, lymphatic, and immunometabolic pathways in lipedema remain insufficiently understood. This preliminary exploratory study evaluated clinical outcomes and circulating mediators during a 7-month LCHF dietary intervention. Twenty-four women with lipedema (median age: 39 years) underwent a 7-month individualized, calorie-restricted LCHF diet under medical supervision. Outcomes included body mass index (BMI), leg volume, and adipose tissue pain assessed using a visual analogue scale (VAS). Fasting serum samples collected at baseline and follow-up were analyzed for angiogenic, inflammatory, endothelial, and lipid mediators using Luminex assays and liquid chromatography-tandem mass spectrometry (LC-MS/MS). The intervention was associated with significant reductions in BMI, leg volume, and adipose tissue pain ( < 0.001). These changes were accompanied by increased vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor D (VEGF-D), and angiopoietin-2 (Ang-2), together with decreased pro-inflammatory cytokines and endothelial adhesion molecules. Several endocannabinoid-related lipid mediators, including oleoyl ethanolamide (OEA), arachidonoyl ethanolamide (AEA), and palmitoyl ethanolamide (PEA), also decreased. Baseline OEA and AEA concentrations, as well as reductions in OEA over time, were associated with greater BMI reduction. Change in interleukin-8 (IL-8) showed a nominal association with leg volume reduction, while pain improvement was associated with decreases in P-selectin and VEGF-A and increases in interleukin-13 (IL-13). A 7-month calorie-restricted LCHF dietary intervention in women with lipedema was associated with clinical improvement and changes in circulating vascular, inflammatory, and lipid mediators. These findings reflect systemic changes accompanying the intervention; however, causal relationships and specific mechanisms cannot be established. - Source: PubMed
Publication date: 2026/04/28
Chachaj AngelikaFleszar MariuszLewandowski ŁukaszFortuna PaulinaMaciejewska GabrielaSowicz MonikaAdaszyńska AgnieszkaJakobsche-Policht UrszulaKrzystek-Korpacka MałgorzataSzuba AndrzejJeziorek Małgorzata - There are relatively well-substantiated concepts regarding the differences in the clinical course of metastatic colorectal cancer depending on the primary tumor localization: right- and left-sided (including rectal). However, many clinical trials demonstrate clear differences in the selected efficacy of adjuvant chemotherapy in the treatment of rectal versus colon cancer. We hypothesize that there are significant differences in long-term outcomes between patients with metastatic rectal cancer (RC) and those with left-sided colon cancer (LSCC) that may depend on the genetic profile of the primary tumor. - Source: PubMed
Publication date: 2026/04/15
Semenov N NZhukova L GYakovlev V A - During the egg laying period of a hen, one pre-hierarchical follicle, approximately 6-8 mm in size, is selected into the preovulatory hierarchy for ovulatory stage development. These follicles develop from white follicles that are 2-5 mm in size. Although numerous studies have investigated follicle selection, the molecular mechanisms underlying pre-hierarchical follicle development and recruitment remain unclear. In this study, we explored the genes regulating chicken ovarian pre-hierarchical follicular development by sequencing RNA from ≤ 2 mm follicles in ovarian stroma (OS), 3-4 mm small white follicles (SWFs), and 6-8 mm small yellow follicles (SYFs) using Oxford Nanopore long-read transcriptome sequencing technology. Herein, we obtained 2,164 differentially expressed transcripts (DETs) from the three phases. The steroidogenesis and angiogenesis signaling pathways were enriched in SWFs compared with in OS. In contrast, the endocytosis, p53, FoxO, and oocyte meiotic signaling pathways were significantly enriched during SYF development compared with during SWF development. The focal adhesion, apelin, and TGF-β signaling pathways were significantly enriched in all three phases. The time-course analysis of DETs and cluster Kyoto Encyclopedia of Genes and Genomes enrichment revealed dynamic changes in gene expression during pre-hierarchical follicle development. Key examples include the genes associated with follicle initial recruitment and development (AMH, GDF9, INHBB, BMPR1B, StAR, and FST), angiogenesis-related genes (ANGPT2, VEGFA, VEGFC, VEGFD, and VEGFRs), extracellular matrix remodeling-related genes (MMP2 and MMP10), and Wnt signaling pathway genes (WNT4, WNT9A, CTNNB1, RSPO3, and WIF1). Moreover, RSPO3 upregulated the expression of FSHR and StAR in cultured chicken Pre-hierarchical follicle granulosa cells and activated the Wnt signaling pathway. The results obtained in this study demonstrate the transcriptional dynamics during small folliculogenesis; the identified signaling pathways and DETs can be used as candidate targets for investigating pre-hierarchical follicle development in chickens. - Source: PubMed
Publication date: 2026/02/18
Cao XiaoyunXu WentingZhang HongruiZhang JialeJiang YunliangLi XianyaoKang Li - The placenta is a highly vascularised organ that depends on tightly regulated angiolymphatic networks to sustain normal fetal growth and maternal adaptation to pregnancy. Disruption of these pathways contributes to major obstetric complications, including preeclampsia, fetal growth restriction, gestational diabetes, and stillbirth. In recent years, advances in molecular pathology and high-throughput technologies have identified a spectrum of angiogenic, lymphangiogenic, and endothelial biomarkers that provide mechanistic insights and hold translational promise. Among these, vascular endothelial growth factors (VEGF-A, VEGF-C, VEGF-D), placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), angiopoietins, podoplanin, and lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) have emerged as key regulators. Differential expression of these markers in placental tissue, maternal circulation, and extracellular vesicles has been correlated with disease severity, placental morphology, and adverse neonatal outcomes. Despite growing evidence, clinical application is limited by methodological heterogeneity, gestational age-specific variability, and incomplete understanding of lymphatic involvement in placental physiology. This review synthesises current knowledge on angiolymphatic biomarkers in the placenta, highlighting their role in vascular development, disease pathogenesis, and potential as diagnostic and prognostic tools. Future research integrating molecular assays, imaging modalities, and systems biology approaches is essential to standardise biomarker panels and translate them into clinically meaningful strategies for maternal-fetal medicine. - Source: PubMed
Publication date: 2025/12/09
Palo SeetuMangla MishuMotwani Rohini