title: Pathophysiology of tumor neovascularization.
abstract: Neovascularization is essential to the process of development and differentiation of tissues in the vertebrate embryo, and is also involved in a wide variety of physiological and pathological conditions in adults, including wound repair, metabolic diseases, inflammation, cardiovascular disorders, and tumor progression. Thanks to cumulative studies on vasculature, new therapeutic approaches have been opened for us to some life-threatening diseases by controlling angiogenesis in the affected organs. In cancer therapy, for example, modulation of factors responsible for tumor angiogenesis may be beneficial in inhibiting of tumor progression. Several antiangiogenic approaches are currently under preclinical trial. However, the mechanisms of neovascularization in tumors are complicated and each tumor shows unique features in its vasculature, depending on tissue specificity, angiogenic micromilieu, grades and stages, host immunity, and so on. For better understanding and effective therapeutic approaches, it is important to clarify both the general mechanism of angiogenic events and the disease-specific mechanism of neovascularization. This review discusses the general features of angiogenesis under physiological and pathological conditions, mainly in tumor progression. In addition, recent topics such as contribution of the endothelial progenitor cells, tumor vasculogenic mimicry, markers for tumor-derived endothelial cells and pericytes, and angiogenic/angiostatic chemokines are summarized.
authors.affiliation: Department of Molecular Pathology, Chiba University Graduate School of Medicine, Chuo-ku, Chiba, Japan. furuya@faculty.chiba-u.jp
authors.forename: Mitsuko
authors.initials: M
authors.lastname: Furuya
authors.forename: Mariko
authors.initials: M
authors.lastname: Nishiyama
authors.forename: Yoshitoshi
authors.initials: Y
authors.lastname: Kasuya
authors.forename: Sadao
authors.initials: S
authors.lastname: Kimura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ishikura
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D042501:Angiogenic Proteins / Q000378:metabolism*; D000818:Animals; D002454:Cell Differentiation; D019070:Cell Lineage; D018925:Chemokines / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005109:Extracellular Matrix / Q000378:metabolism; D005346:Fibroblast Growth Factors / Q000378:metabolism; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D009369:Neoplasms / Q000098:blood supply* / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020286:Pericytes / Q000378:metabolism / Q000473:pathology; D020710:RGS Proteins / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D015398:Signal Transduction; D013234:Stem Cells / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D020533:Angiogenesis Inhibitors; D042501:Angiogenic Proteins; D018925:Chemokines; D020710:RGS Proteins; D043562:Receptors, G-Protein-Coupled; D042461:Vascular Endothelial Growth Factor A; D005346:Fibroblast Growth Factors