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Journal articles on the topic 'Angiogenesis'

To see the other types of publications on this topic, follow the link: Angiogenesis.

Author: Grafiati

Published: 4 June 2021

Last updated: 7 July 2024

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1

Budhraja, Mridula, Rashmi Wardhan, and Keerti Jain Behera. "Continuous Models of Tumor Induced Angiogenesis and Anti-Angiogenesis Strategy." Mathematical Journal of Interdisciplinary Sciences 2, no. 1 (September 2, 2013): 57–75. http://dx.doi.org/10.15415/mjis.2013.21005.

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2

Lee, Hyun Ji, Yong Jun Hong, and Miri Kim. "Angiogenesis in Chronic Inflammatory Skin Disorders." International Journal of Molecular Sciences 22, no. 21 (November 7, 2021): 12035. http://dx.doi.org/10.3390/ijms222112035.

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Angiogenesis, the growth of new blood vessels from preexisting vessels, is associated with inflammation in various pathological conditions. Well-known angiogenetic factors include vascular endothelial growth factor (VEGF), angiopoietins, platelet-derived growth factor, transforming growth factor-β, and basic fibroblast growth factor. Yes-associated protein 1 (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) have recently been added to an important angiogenic factor. Accumulating evidence indicates associations between angiogenesis and chronic inflammatory skin diseases. Angiogenesis is deeply involved in the pathogenesis of psoriasis. VEGF, angiopoietins, tumor necrosis factor-a, interleukin-8, and interleukin-17 are unregulated in psoriasis and induce angiogenesis. Angiogenesis may be involved in the pathogenesis of atopic dermatitis, and in particular, mast cells are a major source of VEGF expression. Angiogenesis is an essential process in rosacea, which is induced by LL-37 from a signal cascade by microorganisms, VEGF, and MMP-3 from mast cells. In addition, angiogenesis by increased VEGF has been reported in chronic urticaria and hidradenitis suppurativa. The finding that VEGF is expressed in inflammatory skin lesions indicates that inhibition of angiogenesis is a useful strategy for treatment of chronic, inflammatory skin disorders.

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3

Tang, Jen-Yang, Yuan-Bin Cheng, Ya-Ting Chuang, Kun-Han Yang, Fang-Rong Chang, Wangta Liu, and Hsueh-Wei Chang. "Oxidative Stress and AKT-Associated Angiogenesis in a Zebrafish Model and Its Potential Application for Withanolides." Cells 11, no. 6 (March 11, 2022): 961. http://dx.doi.org/10.3390/cells11060961.

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Oxidative stress and the AKT serine/threonine kinase (AKT) signaling pathway are essential regulators in cellular migration, metastasis, and angiogenesis. More than 300 withanolides were discovered from the plant family Solanaceae, exhibiting diverse functions. Notably, the relationship between oxidative stress, AKT signaling, and angiogenesis in withanolide treatments lacks comprehensive understanding. Here, we summarize connecting evidence related to oxidative stress, AKT signaling, and angiogenesis in the zebrafish model. A convenient vertebrate model monitored the in vivo effects of developmental and tumor xenograft angiogenesis using zebrafish embryos. The oxidative stress and AKT-signaling-modulating abilities of withanolides were highlighted in cancer treatments, which indicated that further assessments of their angiogenesis-modulating potential are necessary in the future. Moreover, targeting AKT for inhibiting AKT and its AKT signaling shows the potential for anti-migration and anti-angiogenesis purposes for future application to withanolides. This particularly holds for investigating the anti-angiogenetic effects mediated by the oxidative stress and AKT signaling pathways in withanolide-based cancer therapy in the future.

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4

Zhu, Dandan, Ruth Muljadi, Siow Teng Chan, Patricia Vosdoganes, Camden Lo, Joanne C. Mockler, Euan M. Wallace, and Rebecca Lim. "Evaluating the Impact of Human Amnion Epithelial Cells on Angiogenesis." Stem Cells International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/4565612.

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The effects of human amnion epithelial cells (hAECs) on angiogenesis remain controversial. It is yet unknown if the presence of inflammation and/or gestational age of hAEC donors have an impact on angiogenesis. In this study, we examined the differences between term and preterm hAECs on angiogenesisin vitroandin vivo. Conditioned media from term hAECs induced the formation of longer huVEC tubules on Matrigel. Both term and preterm hAECs expressedVEGFA,PDGFB, ANGPT1,andFOXC1, which significantly increased after TNFαand IFNγstimulation. In the presence of TNFαand IFNγ, coculture with term hAECs reduced gene transcription ofTie-2andFoxc1in huVECs, while coculture with preterm hAECs increased gene transcription ofPDGFRαandPDGFRβand reduced gene transcription ofFOXC1in huVECs.In vivoassessment of angiogenesis using vWF immunostaining revealed that hAEC treatment decreased angiogenesis in a bleomycin model of lung fibrosis but increased angiogenesis in a neonatal model of hyperoxia-induced lung injury. In summary, our findings suggested that the impact of hAECs on angiogenesis may be influenced by the presence of inflammation and underlying pathology.

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5

Lazarov, Nikolai, and Faisal Saghir. "AN INSIGHT INTO ENDOMETRIOSIS: ROLE AND INFLUENCE OF THE PROCESS OF ANGIOGENESISS." Journal of IMAB - Annual Proceeding (Scientific Papers) 30, no. 1 (January 23, 2024): 5323–27. http://dx.doi.org/10.5272/jimab.2024301.5323.

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Introduction: Endometriosis is one of the most common gynaecological disorders present in females. According to the implantation of ectopic endometrial tissue outside of the uterine cavity, angiogenesis is an essential prerequisite for the progression of the disease. The purpose is to provide insight and a better understanding of the role that angiogenetic factors play within endometriosis and how this can translate into more effective diagnostic and therapeutic approaches taken by medical specialists when treating this disease. Materials and methods: We conducted a review of the available scientific literature on PubMed, Google Scholar and Science Direct, which included randomized controlled trials, observational studies, prospective controlled studies and case reports. Results and Discussion: Our review of the scientific literature showed that the role of angiogenesis upon the development of endometrial ectopic tissue is very significant, and a positive relationship is established with an increase in neo-angiogenesis and a quicker rate of development of ectopic endometrial tissue. We also found data indicating that there are a multitude of angiogenetic and anti-angiogenetic factors functioning in a homeostatic manner to provide an optimal environment for the endometrial tissue to proliferate and for translocation for the implantation of the ectopic tissue within different locations both within the uterine cavity and distant anatomical locations and regions located outside of the uterine cavity. Conclusion: Recently, the research surrounding the process of angiogenesis is positive and positive correlations have been established between the role of angiogenesis and the extent to which the ectopic endometrial tissue proliferates.

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6

Aziz, Shiekh Aejaz. "Angiogenesis and Cancer." JMS SKIMS 12, no. 2 (December 13, 2009): 32–33. http://dx.doi.org/10.33883/jms.v12i2.11.

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Tumors measuring 1-2 (mm)3 lack blood supply and neovascularization is a major process orchestrated by over-production and release of pro-angiogenic growth factors causing sequential step-wise formation of blood vessel capillaries in tumors.Moleculars mediators of tumors angiogenesis include VEGF family, IL-8, EGF receptor ligands, basic and acidic FGF, PDGF etc. There are natural endogenenous inhibitors of tumorigenesis (TSP-1,Vasostatin).Negative feedback mechanisms do exist to control/regulate tumor angiogenesis. Angiogeneis is detrimental to tumor progression favouring transition from hyperplasia to a neoplastic state, influencing cancer cell dissemination besides exerting an independent negative prognosis. Tumor vasculature is dysfunctional, heterogeneous in the tumor mass interms of density leading to a limited/retarded diffusion of drugs especially certain antibodies,gene therapy vectors, immune-effector cells through interstitium of these tumors. The hypoxic zones in tumors are the areas of resistance to the chemotherapy. Angiogenesis is upregulated in tumorigenesis leading to over-production of proangiogenic growth factors that have become targets for anticancer drug development. J Med Sci.2009;12(2):32-33

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7

Gammone, Maria A., Antonella Danese, and Nicolantonio D’Orazio. "Anti-Angiogenetic Agents from the Sea: A New Potential Preventive and Therapeutic Wave?" Anti-Cancer Agents in Medicinal Chemistry 20, no. 17 (November 12, 2020): 2005–11. http://dx.doi.org/10.2174/1871520620666200705215226.

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: Angiogenesis, generation of novel blood vessels from pre-existing ones, is a prerequisite for the physiological expansion, reparation, and functioning of body tissues and systems. However, it is also involved in some pathological inflammatory situations, such as oncologic and chronic degenerative disorders. The correct angiogenesis and neo-vascular response also accompanies wound healing, interaction with biocompatible materials, and tissue regeneration. : In this respect, natural products deriving from terrestrial and marine plants/organisms may prevent and even cure various angiogenesis-dependent disorders. : Bioactive natural compounds with antioxidant and anti-inflammatory activities could concur to maintain adequate vascularization and endothelial functions and inhibit angiogenesis, thus controlling tumor development. : This review aims to illustrate the role of some marine-derived compounds as anti-angiogenetic agents.

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8

Zhu, Jianlin, Lu Wang, Fan Liu, Jinghua Pan, Zhimeng Yao, Yusheng Lin, Yabing Yang, et al. "Targeting PELP1 Attenuates Angiogenesis and Enhances Chemotherapy Efficiency in Colorectal Cancer." Cancers 14, no. 2 (January 13, 2022): 383. http://dx.doi.org/10.3390/cancers14020383.

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Abnormal angiogenesis is one of the important hallmarks of colorectal cancer as well as other solid tumors. Optimally, anti-angiogenesis therapy could restrain malignant angiogenesis to control tumor expansion. PELP1 is as a scaffolding oncogenic protein in a variety of cancer types, but its involvement in angiogenesis is unknown. In this study, PELP1 was found to be abnormally upregulated and highly coincidental with increased MVD in CRC. Further, treatment with conditioned medium (CM) from PELP1 knockdown CRC cells remarkably arrested the function of human umbilical vein endothelial cells (HUVECs) compared to those treated with CM from wildtype cells. Mechanistically, the STAT3/VEGFA axis was found to mediate PELP1-induced angiogenetic phenotypes of HUVECs. Moreover, suppression of PELP1 reduced tumor growth and angiogenesis in vivo accompanied by inactivation of STAT3/VEGFA pathway. Notably, in vivo, PELP1 suppression could enhance the efficacy of chemotherapy, which is caused by the normalization of vessels. Collectively, our findings provide a preclinical proof of concept that targeting PELP1 to decrease STAT3/VEGFA-mediated angiogenesis and improve responses to chemotherapy due to normalization of vessels. Given the newly defined contribution to angiogenesis of PELP1, targeting PELP1 may be a potentially ideal therapeutic strategy for CRC as well as other solid tumors.

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9

Hansen, Torben Frøstrup, Camilla Qvortrup, and Per Pfeiffer. "Angiogenesis Inhibitors for Colorectal Cancer. A Review of the Clinical Data." Cancers 13, no. 5 (March 1, 2021): 1031. http://dx.doi.org/10.3390/cancers13051031.

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Since the late 1990s, therapy for metastatic colorectal cancer (mCRC) has changed considerably, and the combination of doublet or triplet chemotherapy and a targeted agent are now routinely used. The targeting of angiogenesis, the development of new blood vessels, represents a key element in the overall treatment strategy. Since the approval in 2004 of the first anti-angiogenetic drug, multiple agents have been approved and others are currently under investigation. We present an overview of the recent literature on approved systemic treatment of mCRC, with a focus on anti-angiogenic drugs, and current treatment approaches, and elaborate on the future role of angiogenesis in colorectal cancer as seen from a clinical perspective. The treatment of mCRC, in general, has changed from “one strategy fits all” to a more personalized approach. This is, however, not entirely the case for anti-angiogenetic treatments, partly due to a lack of validated biomarkers. The anti-angiogenetic standard treatment at the present primarily includes monoclonal antibodies. The therapeutic field of angiogenesis, however, has received increased interest after the introduction of newer combinations. These approaches will likely change the current treatment strategy, once again, to the overall benefit of patients.

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10

Miyazawa, Teruo, and Akira Shibata. "Angiogenesis." Nippon Shokuhin Kagaku Kogaku Kaishi 56, no. 8 (2009): 467. http://dx.doi.org/10.3136/nskkk.56.467.

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11

Adair, Thomas H., and Jean-Pierre Montani. "Angiogenesis." Colloquium Series on Integrated Systems Physiology: From Molecule to Function 2, no. 1 (January 2010): 1–84. http://dx.doi.org/10.4199/c00017ed1v01y201009isp010.

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12

Lomberk, Gwen. "Angiogenesis." Pancreatology 10, no. 2-3 (June 2010): 112–13. http://dx.doi.org/10.1159/000297465.

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13

Senger, D. R., and G. E. Davis. "Angiogenesis." Cold Spring Harbor Perspectives in Biology 3, no. 8 (August 1, 2011): a005090. http://dx.doi.org/10.1101/cshperspect.a005090.

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14

Ergul, Adviye, Ahmed Alhusban, and Susan C. Fagan. "Angiogenesis." Stroke 43, no. 8 (August 2012): 2270–74. http://dx.doi.org/10.1161/strokeaha.111.642710.

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15

Zhao, Qiang, and Zongjin Li. "Angiogenesis." BioMed Research International 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/135861.

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16

Folkman, Judah. "Angiogenesis." Annual Review of Medicine 57, no. 1 (February 2006): 1–18. http://dx.doi.org/10.1146/annurev.med.57.121304.131306.

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17

Terjung, R. L., R. J. Tomanek, T. L. Haas, P. D. Wagner, and O. Hudlicka. "ANGIOGENESIS." Medicine & Science in Sports & Exercise 34, no. 5 (May 2002): S212. http://dx.doi.org/10.1097/00005768-200205001-01184.

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18

POST, MARK J. "Angiogenesis." Annals of the New York Academy of Sciences 961, no. 1 (June 2002): 249–50. http://dx.doi.org/10.1111/j.1749-6632.2002.tb03093.x.

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19

Simons, Michael. "Angiogenesis." Circulation 111, no. 12 (March 29, 2005): 1556–66. http://dx.doi.org/10.1161/01.cir.0000159345.00591.8f.

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20

Swerlick, Robert A. "Angiogenesis." Journal of Dermatology 22, no. 11 (November 1995): 845–52. http://dx.doi.org/10.1111/j.1346-8138.1995.tb03934.x.

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21

Zetter, Bruce R. "Angiogenesis." Chest 93, no. 3 (March 1988): 159S—166S. http://dx.doi.org/10.1378/chest.93.3_supplement.159s.

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22

Munoz, David G., and John M. Woulfe. "Angiogenesis." Neurology 85, no. 21 (October 28, 2015): 1826–27. http://dx.doi.org/10.1212/wnl.0000000000002160.

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23

Kuwano, Michihiko, Mayumi Ono, and Kiinnoshi Kohnn. "Angiogenesis." Japanese Journal of Pharmacology 67 (1995): 65. http://dx.doi.org/10.1016/s0021-5198(19)46230-6.

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24

Folkman, J., and Y. Shing. "Angiogenesis." Journal of Biological Chemistry 267, no. 16 (June 1992): 10931–34. http://dx.doi.org/10.1016/s0021-9258(19)49853-0.

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25

Pircher, Andreas. "Angiogenesis." memo - Magazine of European Medical Oncology 7, no. 4 (December 2014): 193. http://dx.doi.org/10.1007/s12254-014-0176-2.

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26

Logan, Ann. "Angiogenesis." Lancet 341, no. 8858 (June 1993): 1467–68. http://dx.doi.org/10.1016/0140-6736(93)90902-s.

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27

&NA;. "Angiogenesis." Journal of Immunotherapy 26, no. 6 (November 2003): S29—S31. http://dx.doi.org/10.1097/00002371-200311000-00010.

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28

DeWitt, Natalie. "Angiogenesis." Nature 438, no. 7070 (December 2005): 931. http://dx.doi.org/10.1038/438931a.

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29

Smith, Stephen. "Angiogenesis." Seminars in Reproductive Medicine 15, no. 03 (August 1997): 221–27. http://dx.doi.org/10.1055/s-2008-1068751.

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30

Sage, Helene. "Angiogenesis." Advances in Dental Research 9, no. 3_suppl (November 1995): 5. http://dx.doi.org/10.1177/0895937495009003s1701.

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31

Kontos, Christopher D., and Brian H. Annex. "Angiogenesis." Current Atherosclerosis Reports 1, no. 2 (September 1999): 165–71. http://dx.doi.org/10.1007/s11883-999-0013-y.

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32

Ondrick, Karen, and Brad G. Samojla. "ANGIOGENESIS." Clinics in Podiatric Medicine and Surgery 9, no. 1 (January 1992): 185–202. http://dx.doi.org/10.1016/s0891-8422(23)00509-8.

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33

SHIBUYA, Masabumi. "Angiogenesis, anti-angiogenesis, and tumor suppression." Folia Pharmacologica Japonica 120, no. 5 (2002): 285–94. http://dx.doi.org/10.1254/fpj.120.285.

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34

Ribatti, D., A. Vacca, B. Nico, G. De Falco, P. Giuseppe Montaldo, and M. Ponzoni. "Angiogenesis and anti-angiogenesis in neuroblastoma." European Journal of Cancer 38, no. 6 (2002): 750–57. http://dx.doi.org/10.1016/s0959-8049(01)00337-9.

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35

Tímár, József, Balázs Döme, Károly Fazekas, Ágnes Janovics, and Sándor Paku. "Angiogenesis-dependent diseases and angiogenesis therapy." Pathology & Oncology Research 7, no. 2 (June 2001): 85–94. http://dx.doi.org/10.1007/bf03032573.

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36

Faihs, Lorenz, Bardia Firouz, Paul Slezak, Cyrill Slezak, Michael Weißensteiner, Thomas Ebner, Nassim Ghaffari Tabrizi-Wizsy, Kurt Schicho, and Peter Dungel. "A Novel Artificial Intelligence-Based Approach for Quantitative Assessment of Angiogenesis in the Ex Ovo CAM Model." Cancers 14, no. 17 (September 1, 2022): 4273. http://dx.doi.org/10.3390/cancers14174273.

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Angiogenesis is a highly regulated process. It promotes tissue regeneration and contributes to tumor growth. Existing therapeutic concepts interfere with different steps of angiogenesis. The quantification of the vasculature is of crucial importance for research on angiogenetic effects. The chorioallantoic membrane (CAM) assay is widely used in the study of angiogenesis. Ex ovo cultured chick embryos develop an easily accessible, highly vascularised membrane on the surface. Tumor xenografts can be incubated on this membrane enabling studies on cancer angiogenesis and other major hallmarks. However, there is no commonly accepted gold standard for the quantification of the vasculature of the CAM. We compared four widely used measurement techniques to identify the most appropriate one for the quantification of the vascular network of the CAM. The comparison of the different quantification methods suggested that the CAM assay application on the IKOSA platform is the most suitable image analysis application for the vasculature of the CAM. The new CAM application on the IKOSA platform turned out to be a reliable and feasible tool for practical use in angiogenesis research. This novel image analysis software enables a deeper exploration of various aspects of angiogenesis and might support future research on new anti-angiogenic strategies for cancer treatment.

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37

Lijuan, Chen, Xu Jiaren, Shuang Wu, Rong Wang, Qu Xiaoyan, Yu Wenjun, and Jianyong Li. "Argonaute2 promotes myeloma angiogenesis by deregulation of microRNAs." Blood 122, no. 21 (November 15, 2013): 5334. http://dx.doi.org/10.1182/blood.v122.21.5334.5334.

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Abstract Dysregulation of miRNAs expression contributes to cancer cell proliferation, apoptosis and angiogenesis. Angiogenesis is a hallmark of multiple myeloma development and progression. Argonaute 2 (AGO2) protein, the core component of RNA-induced silencing complex (RISC), can directly bind miRNAs and mediate target mRNAs degradation. Previous study showed that AGO2 knockdown suppressed the growth and tube formation of HUVECs. In current study, the supernatant of AGO2 over-expression MM lines could induce HUVECs migration and accelerated tube formation. Conversely, the supernatant of AGO2 knockdown MM lines could suppress cell migration and tube formation of HUVECs. Moreover, CAM assay also demonstrated AGO2 can drive neovessel formation of MM in vivo. Using miRNAs microarray, we observed that 25 miRNAs were up-regulated and 14 miRNAs were down-regulated by AGO2 protein. Among these AGO2-associated miRNAs, most Let-7 family and two miR-17-92 cluster members (miR-17a and miR-92-1), known as pro-angiogenetic miRNAs, were the dominant positively regulated miRNAs by AGO2, and the anti-angiogenetic miRNAs, such as miR-145 and miR-361 were inversely regulated by AGO2 protein, which play crucial role in AGO2 mediating angiogenesis. Disclosures: No relevant conflicts of interest to declare.

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38

Takakura, Nobuyuki. "Angiogenesis: Regulation of angiogenesis by hematopoietic cells." Ensho Saisei 24, no. 5 (2004): 553–61. http://dx.doi.org/10.2492/jsir.24.553.

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39

Ribatti, D., and A. Vacca. "Angiogenesis and anti-angiogenesis in haematological diseases." memo - Magazine of European Medical Oncology 1, no. 1 (March 2008): 31–33. http://dx.doi.org/10.1007/s12254-008-0008-3.

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40

Ribatti, Domenico, Angelo Vacca, Beatrice Nico, Domenico Sansonno, and Franco Dammacco. "Angiogenesis and anti-angiogenesis in hepatocellular carcinoma." Cancer Treatment Reviews 32, no. 6 (October 2006): 437–44. http://dx.doi.org/10.1016/j.ctrv.2006.06.002.

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41

Schweigerer, Lothar, and Theodor Fotsis. "Angiogenesis and angiogenesis inhibitors in paediatric diseases." European Journal of Pediatrics 151, no. 7 (July 1992): 472–76. http://dx.doi.org/10.1007/bf01957746.

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42

Ribatti, Domenico, Angelo Vacca, Franco Dammacco, and Denis English. "Angiogenesis and Anti-Angiogenesis in Hematological Malignancies." Journal of Hematotherapy & Stem Cell Research 12, no. 1 (February 2003): 11–22. http://dx.doi.org/10.1089/152581603321210091.

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43

NAKASHIMA, Yutaka. "Angiogenesis and Regulating Factors." Journal of Japan Atherosclerosis Society 16, no. 7 (1988): 917–20. http://dx.doi.org/10.5551/jat1973.16.7_917.

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44

Loron, Gauthier, Julien Pansiot, Paul Olivier, Christiane Charriaut-Marlangue, and Olivier Baud. "Inhaled Nitric Oxide Promotes Angiogenesis in the Rodent Developing Brain." International Journal of Molecular Sciences 24, no. 6 (March 20, 2023): 5871. http://dx.doi.org/10.3390/ijms24065871.

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Inhaled nitric oxide (iNO) is a therapy used in neonates with pulmonary hypertension. Some evidence of its neuroprotective properties has been reported in both mature and immature brains subjected to injury. NO is a key mediator of the VEGF pathway, and angiogenesis may be involved in the reduced vulnerability to injury of white matter and the cortex conferred by iNO. Here, we report the effect of iNO on angiogenesis in the developing brain and its potential effectors. We found that iNO promotes angiogenesis in the developing white matter and cortex during a critical window in P14 rat pups. This shift in the developmental program of brain angiogenesis was not related to a regulation of NO synthases by exogenous NO exposure, nor the VEGF pathway or other angiogenic factors. The effects of iNO on brain angiogenesis were found to be mimicked by circulating nitrate/nitrite, suggesting that these carriers may play a role in transporting NO to the brain. Finally, our data show that the soluble guanylate cyclase/cGMP signaling pathway is likely to be involved in the pro-angiogenetic effect of iNO through thrombospondin-1, a glycoprotein of the extracellular matrix, inhibiting soluble guanylate cyclase through CD42 and CD36. In conclusion, this study provides new insights into the biological basis of the effect of iNO in the developing brain.

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45

Würdinger, Thomas, and Bakhos A. Tannous. "Glioma angiogenesis." Cell Adhesion & Migration 3, no. 2 (April 2009): 230–35. http://dx.doi.org/10.4161/cam.3.2.7910.

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46

Simons, Michael, Roger J. Laham, Mark Post, and Frank W. Sellke. "Therapeutic Angiogenesis." BioDrugs 14, no. 1 (July 2000): 13–20. http://dx.doi.org/10.2165/00063030-200014010-00002.

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47

&NA;. "Therapeutic angiogenesis." Inpharma Weekly &NA;, no. 1191 (June 1999): 2. http://dx.doi.org/10.2165/00128413-199911910-00002.

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48

Kaur, Mandeep. "Targeting Angiogenesis." International Journal of Head and Neck Surgery 5, no. 2 (2014): 78–86. http://dx.doi.org/10.5005/jp-journals-10001-1186.

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ABSTRACT Blood vessels constitute the first organ in the embryo and form the largest network in the body, but sadly are often deadly. Angiogenesis is the process of generating new capillary blood vessels. Vasculogenesis is the term used for spontaneous bloodvessel formation, and intussusception is the term for new blood vessel formation by splitting off existing ones. Angiogenesis is a normal and vital process in growth and development, as well as in wound healing and in granulation tissue. It is also a fundamental step in the transition of tumors from a dormant state to a malignant one, leading to the use of angiogenesis inhibitors. Angiogenesis may be a target for combating diseases characterized by either poor vascularization or abnormal vasculature. Application of specific compounds that may inhibit or induce the creation of new blood vessels in the body may help combat such diseases. In this review, we will present an overview of the knowledge gained in studies related to the identification and characterization of different inhibitors and regulators of angiogenesis and also to highlight briefly the pathological and physiological angiogenesis. How to cite this article Kaur M. Targeting Angiogenesis. Int J Head Neck Surg 2014;5(2):78-86.

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49

KUWANO, Michihiko, Jun-ichi FUKUSHI, Masahiro OKAMOTO, Akihiro NISHIE, Hisatsugu GOTO, Tatsuro ISHIBASHI, and Mayumi ONO. "Angiogenesis Factors." Internal Medicine 40, no. 7 (2001): 565–72. http://dx.doi.org/10.2169/internalmedicine.40.565.

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50

Ryan, Charles J., and George Wilding. "Angiogenesis Inhibitors." Drugs & Aging 17, no. 4 (October 2000): 249–55. http://dx.doi.org/10.2165/00002512-200017040-00001.

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