PubAngioGen is a database dedicated to Angiogenesis which is a process of generating new blood vessels based on existing ones, and is involved in many diseases. Through manual text-mining, we extracted those published results related to angiogenesis at multi-levels, including molecular, cell, animal model and disease, and comprehensively summarized the relationship between angiogenesis and major diseases, which provides the latest information of angiogenesis involved in main diseases and signaling pathways.
Considering that the compounds or proteins which promote or inhibit the pathological angiogenesis can be potential new drugs, we also collected those potential drug targets and related compounds that are proved to be effect on angiogenesis. In addition, we collected those candidates of angiogenic factors that are in clinical trials and the therapeutic targets for anti-angiogenic or pro-angiogenic drug development.
Our database provides the first integrated resources for exploring the relationships between angiogenesis and diseases, such as cancers, diabetes, cardiovascular diseases, as well as related research progresses for drug development.
Angiogenesis results in the formation of new blood vessels. Tumor growth, tissue wound and inflammation can induce angiogenesis. Rapid tumor cell growth creates intracellular hypoxia, which initiates a series of cell signaling events that promote angiogenesis. Hypoxia-inducible factor (HIF) is a transcription factor that responds to changing intracellular oxygen concentration. Under typical oxygen levels (normoxia), HIF is hydroxylated and acetylated, modifications that target the transcription factor for VHL mediated ubiquitin degradation. During hypoxia, HIF accumulates and is transported to the nucleus where it induces expression of a wide variety of target gene products, including proteins important for inducing tumor endothelial cell angiogenesis. Growth factors (such as VEGF, FGF, and TGF) induce signaling pathways (including PLC¶√, PI3K, Src, Smad signaling) that result in endothelial cell proliferation, increase vascular permeability and cell migration. Extracellular matrix proteases and regulators induce tissue matrix remodeling in preparation for migration of endothelial cells from existing vessels to form new tubing. Cytokines promote additional tumor growth and induce the expression of signaling proteins (i.e. Slit2) that promote the creation of tumor-associated blood vessels. In addition to hypoxia, PI3K and Ras pathways can increase HIF expression by promoting HIF translation. Tissue wounding, ischemia or inflammation recruit macrophage and bone marrow-derived inflammatory cells (BDMC) to wound areas, where these monocytes induce a similar panel of secreted proteins to induce angiogenesis.
Node annotation information
Angiogenesis is a complicated process of generating new blood vessels based on existing ones. In order to better elucidate the underlying mechanism of angiogenesis, our database includes lots of resources related to angiogenesis at multi-levels, including molecular, cell, animal model and disease and integrates compounds, genes, proteins, signal transduction and disease closely. In the network, each node represents a gene/protein or the compound that target the proteins. We also provide related functions in order to facilitate the users to query their relationships.
For the purpose of maximally displaying annotation information and optimizing web data transmission, we developed the online display tools, which provide more detailed network information output and have some online analysis functions. User can analyze the query in the global view.
PubAngioGen provides manually collected relationships between angiogenesis/diseases and protein/compound data and predicted information through synthetic data resources. Users can access information by querying proteins or compounds (http://www.megabionet.org/aspd/query.php). The web site allows users to submit the name of protein/compound/disease when you would like to know their roles in angiogenesis. All returned pages will tell users the related useful annotations of all proteins involved in certain interactive pathways. Additionally, query keywords, including UniProtKB/Swiss-Prot ID, Entrez Gene name or REFSEQ PROVISIONAL ID (NCBI), are all allowed.