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1 Pathology and Molecular and Cellular Physiology, LSU Health Sciences Center-Shreveport, Shreveport, Louisiana, United States
2 Pathology, LSU Health Sciences Center-Shreveport, Shreveport, Louisiana, United States
3 Mol & Cell Physiol, LSU Health Sci Ctr, Louisiana, United States
4 Department of Pathology, Louisiana State University, 1501 Kings Highway, Shreveport, Louisiana, 71130, United States; Department of Pathology and Molecular and Cellular Physiology, Louisiana State University, Shreveport, Louisiana, United States
* To whom correspondence should be addressed. E-mail: ckevil{at}lsuhsc.edu.
Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that these factors develop simultaneously over time as disease progresses and correlated in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon including; growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that anti-angiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed.
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