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      The extracellular matrix and blood vessel formation: not just a scaffold

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          Abstract

          The extracellular matrix plays a number of important roles, among them providing structural support and information to cellular structures such as blood vessels imbedded within it. As more complex organisms have evolved, the matrix ability to direct signalling towards the vasculature and remodel in response to signalling from the vasculature has assumed progressively greater importance. This review will focus on the molecules of the extracellular matrix, specifically relating to vessel formation and their ability to signal to the surrounding cells to initiate or terminate processes involved in blood vessel formation.

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          Angiogenesis in life, disease and medicine.

          Peter Carmeliet (2005)
          The growth of blood vessels (a process known as angiogenesis) is essential for organ growth and repair. An imbalance in this process contributes to numerous malignant, inflammatory, ischaemic, infectious and immune disorders. Recently, the first anti-angiogenic agents have been approved for the treatment of cancer and blindness. Angiogenesis research will probably change the face of medicine in the next decades, with more than 500 million people worldwide predicted to benefit from pro- or anti-angiogenesis treatments.
          Article 0 comments Cited 797 times – based on 0 reviews     Review now
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            Molecular regulation of vessel maturation.

            Rakesh Jain (2003)
            The maturation of nascent vasculature, formed by vasculogenesis or angiogenesis, requires recruitment of mural cells, generation of an extracellular matrix and specialization of the vessel wall for structural support and regulation of vessel function. In addition, the vascular network must be organized so that all the parenchymal cells receive adequate nutrients. All of these processes are orchestrated by physical forces as well as by a constellation of ligands and receptors whose spatio-temporal patterns of expression and concentration are tightly regulated. Inappropriate levels of these physical forces or molecules produce an abnormal vasculature--a hallmark of various pathologies. Normalization of the abnormal vasculature can facilitate drug delivery to tumors and formation of a mature vasculature can help realize the promise of therapeutic angiogenesis and tissue engineering.
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              VEGF as a Key Mediator of Angiogenesis in Cancer

              Peter Carmeliet (2005)
              Vascular endothelial growth factor (VEGF) is a homodimeric glycoprotein with a molecular weight of approximately 45 kDa. It is the key mediator of angiogenesis (the formation of new blood vessels), and binds two VEGF receptors (VEGF receptor-1 and VEGF receptor-2), which are expressed on vascular endothelial cells. In healthy humans, VEGF promotes angiogenesis in embryonic development and is important in wound healing in adults. VEGF is the key mediator of angiogenesis in cancer, in which it is up-regulated by oncogene expression, a variety of growth factors and also hypoxia. Angiogenesis is essential for cancer development and growth: before a tumor can grow beyond 1–2 mm, it requires blood vessels for nutrients and oxygen. The production of VEGF and other growth factors by the tumor results in the ‘angiogenic switch’, where new vasculature is formed in and around the tumor, allowing it to grow exponentially. Tumor vasculature formed under the influence of VEGF is structurally and functionally abnormal. Blood vessels are irregularly shaped, tortuous, have dead ends and are not organized into venules, arterioles and capillaries. They are also leaky and hemorrhagic, which leads to high interstitial pressure. These characteristics mean that tumor blood flow is suboptimal, resulting in hypoxia and further VEGF production. This central role of VEGF in the production of tumor vasculature makes it a rational target for anticancer therapy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (publisher-id): jcmm
                Title: Journal of Cellular and Molecular Medicine
                Publisher: Blackwell Publishing Ltd (Oxford, UK )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Print): March 2007
                Publication date (Electronic): 1 May 2007
                Volume: 11
                Issue: 2
                Pages: 176-205
                Affiliations
                Angiogenesis Research Center, Section of Cardiology, Departments of Medicine and Pharmacology & Toxicology, Dartmouth Medical School, Lebanon, NH, USA
                Author notes
                *Correspondence to: Michael SIMONS Section of Cardiology, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756, USA.; Tel.: 603 650 3540; E-mail: michael.simons@ 123456dartmouth.edu

                Guest Editor: N.I. Moldovan

                Article
                DOI: 10.1111/j.1582-4934.2007.00031.x
                PMC ID: 3822822
                PubMed ID: 17488472
                SO-VID: 14ab6c25-2a3f-4797-8afd-2aad91370761
                History
                Date received : 22 January 2007
                Date accepted : 19 February 2007
                Categories
                Subject: Reviews

                ScienceOpen disciplines: Molecular medicine
                Keywords: extracellular matrix,blood vessel formation,angiogenesis
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: extracellular matrix, blood vessel formation, angiogenesis

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