Special Issue "Angiogenesis Inhibitors"
A special issue of Pharmaceuticals (ISSN 1424-8247).
Deadline for manuscript submissions: closed (30 April 2011)
Prof. Dr. Domenico Ribatti
Dipartimento di Scienze Mediche di Base,Sezione di Anatomia Umana e Istologia, Università degli Studi di Bari, Piazza G. Cesare 11, Policlinico, 70124 Bari, Italy
Phone: +39 080 5478240
Fax: +39 080 5478310
The idea of targeting angiogenesis to inhibit tumor growth was proposed more than three decades ago by Judah Folkman, and since then several approaches to block or disrupt tumor angiogenesis have been explored.
Antiangiogenesis remains a dynamic and evolving field in oncology. New therapeutic targets continue to emerge followed by the rapid development of new therapeutic agents to be investigated in clinical trials.
Until now, the success of antiangiogenic compounds in the clinic is rather limited when given as monotherapies. This is in contrast with many preclinical results which revealed a much higher efficacy of these agents in animal models.
Prof. Dr. Domenico Ribatti
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pharmaceuticals is an international peer-reviewed Open Access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- angiopoietin-2 antagonists
- antiangiogenic monoclonal antibodies
- assays to validate antiangiogenic agents
- biomarkers of response to antiangiogenic therapy
- combination of antiangiogenic therapy with other anticancer therapies
- endogenous inhibitors of angiogenesis
- genetic strategies for targeting angiogenesis
- imaging of tumor angiogenesis
- integrins as targets for antiangiogenic therapy
- metronomic low-dose antiangiogenic chemotherapy
- protein tyrosine kinase inhibitors
- targeted drug delivery to the tumor neovasculature
- thalidomide and its IMiD derivatives
- translating angiogenesis inhibitors to the clinic
Review: The Vasohibin Family
Pharmaceuticals 2010, 3(2), 433-440; doi:10.3390/ph3020433
Received: 13 January 2010; in revised form: 23 January 2010 / Accepted: 3 February 2010 / Published: 5 February 2010| Download PDF Full-text (103 KB)
Pharmaceuticals 2010, 3(3), 482-513; doi:10.3390/ph3030482
Received: 12 January 2010; in revised form: 29 January 2010 / Accepted: 2 March 2010 / Published: 8 March 2010| Download PDF Full-text (219 KB)
Review: Platelet-Derived Growth Factor (PDGF)/PDGF Receptors (PDGFR) Axis as Target for Antitumor and Antiangiogenic Therapy
Pharmaceuticals 2010, 3(3), 572-599; doi:10.3390/ph3030572
Received: 28 January 2010; in revised form: 16 February 2010 / Accepted: 9 March 2010 / Published: 11 March 2010| Download PDF Full-text (2001 KB) | Download XML Full-text
Review: Thrombospondin-1 as a Paradigm for the Development of Antiangiogenic Agents Endowed with Multiple Mechanisms of Action
Pharmaceuticals 2010, 3(4), 1241-1278; doi:10.3390/ph3041241
Received: 14 February 2010; in revised form: 20 April 2010 / Accepted: 22 April 2010 / Published: 23 April 2010| Download PDF Full-text (1390 KB)
Pharmaceuticals 2010, 3(10), 3021-3039; doi:10.3390/ph3103021
Received: 10 August 2010; in revised form: 19 September 2010 / Accepted: 25 September 2010 / Published: 28 September 2010| Download PDF Full-text (404 KB)
Pharmaceuticals 2011, 4(6), 782-793; doi:10.3390/ph4060782
Received: 25 April 2011; in revised form: 23 May 2011 / Accepted: 30 May 2011 / Published: 31 May 2011| Download PDF Full-text (369 KB) | Download XML Full-text
Article: Vasoinhibins Prevent Bradykinin-Stimulated Endothelial Cell Proliferation by Inactivating eNOS via Reduction of both Intracellular Ca2+ Levels and eNOS Phosphorylation at Ser1179
Pharmaceuticals 2011, 4(7), 1052-1069; doi:10.3390/ph4071052
Received: 29 April 2011; in revised form: 6 July 2011 / Accepted: 19 July 2011 / Published: 20 July 2011| Download PDF Full-text (476 KB) | Download XML Full-text
Review: Proteolytically Derived Endogenous Angioinhibitors Originating from the Extracellular Matrix
Pharmaceuticals 2011, 4(12), 1551-1577; doi:10.3390/ph4121551
Received: 14 October 2011; in revised form: 24 November 2011 / Accepted: 25 November 2011 / Published: 2 December 2011| Download PDF Full-text (789 KB) | Download XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Endogenous Matrix-Derived Inhibitors of Angiogenesis
Authors: Malin Sund, Pia Nyberg and Hans P. Eikesdal
Abstract: Endogenous inhibitors of angiogenesis are proteins or fragments of proteins that are formed in the body, which subsequently can inhibit the angiogenic process. These substances can be found both in the circulation and sequestered in the extracellular matrix (ECM) surrounding cells. Many matrix-derived inhibitors of angiogenesis, such as endostatin, tumstatin, canstatin and arresten, are bio-active fragments of larger ECM molecules. These substances become released upon proteolysis of the ECM and the vascular basement membrane (VBM) by enzymes of the tumor microenvironment. Although the role of matrix-derived angiogenesis inhibitors is well studied in animal models of cancer, their role in human cancers is less established. We will in this review discuss the current knowledge about these substances and the potential use of them as tumor therapeutics and/or biomarkers.
Type of Paper: Article
Title: Vasoinhibins and Endothelial Cell Proliferation
Authors: Stéphanie Thebault 1, Carmen González 1, Celina García1, David Arredondo Zamarripa 1, Gabriel Nava 1, Luis Vaca 2, Gonzalo Martínez de la Escalera 1 and Carmen Clapp 1
Affiliations: 1 Instituto de Neurobiología, Universidad Nacional Autónoma de México, Querétaro, Querétaro, 76230, México
2 Departamento de Biología Celular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad Universitaria, Del. Coyoacán, 04510 México, D.F., México; E-Mails: firstname.lastname@example.org (C.C.); email@example.com (S.T.)
Abstract: Vasoinhibins, a family of antiangiogenic peptides derived from prolactin proteolysis, inhibit the vascular effects of several proangiogenic factors, including bradykinin (BK). Here, we report that vasoinhibins block the BK-induced proliferation of bovine umbilical vein endothelial cells.
Inactivation of endothelial nitric oxide synthase (eNOS) mediates this effect, as the NO donor DETA-NONOate prevented vasoinhibin action. Normally, the increase of intracellular Ca2+ levels ([Ca2+]i) upon BK stimulation activates eNOS, and vasoinhibins blocked the BK-mediated activation of phospholipase C and the formation of inositol 1,4,5-triphosphate leading to a reduced release of Ca2+ from intracellular stores. The [Ca2+]i rise evoked by BK also involves the influx of extracellular Ca2+ via transient receptor potential canonical (TRPC) channels. Vasoinhibins likely interfere with TRPC-mediated Ca2+ entry, since La(3+), an enhancer of TRPC4 and TRPC5 channel activity, prevented vasoinhibins from blocking the stimulation by BK of NO production and proliferation, and vasoinhibins reduced the BK-induced increase of TRPC5 mRNA expression. Finally, vasoinhibins prevented the BK-induced phosphorylation of eNOS at Ser1179, a post-translational modification that facilitates Ca2+-calmodulin activation of eNOS. Together, our data show that vasoinhibins, by lowering NO production through the inhibition of both [Ca2+]i mobilization and eNOS phosphorylation, prevent the BK-induced stimulation of endothelial cell proliferation. These mechanisms may help to regulate BK effects on angiogenesis and vascular homeostasis.
Last update: 11 February 2011