Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues.
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 initiating factors for these responses simultaneously increase as disease progresses and correlate 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 antiangiogenic 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.
Chidlow
John H
JH
Department of Pathology, LSU Health Sciences Center-Shreveport, 1501 Kings Highway, Shreveport, LA 71130, USA.
Shukla
Deepti
D
Grisham
Matthew B
MB
Kevil
Christopher G
CG
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D015820:Cadherins / Q000502:physiology; D015815:Cell Adhesion Molecules; D003092:Colitis / Q000503:physiopathology*; D003106:Colon / Q000737:chemistry; D004195:Disease Models, Animal; D006801:Humans; D007136:Immunoglobulins / Q000502:physiology; D018836:Inflammation Mediators / Q000502:physiology; D015212:Inflammatory Bowel Diseases / Q000473:pathology* / Q000628:therapy*; D039564:Integrin alphaV / Q000187:drug effects / Q000502:physiology; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D020782:Matrix Metalloproteinases / Q000502:physiology; D051379:Mice; D008833:Microcirculation; D009088:Mucoproteins / Q000502:physiology; D009389:Neovascularization, Pathologic / Q000517:prevention & control; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000502:physiology; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology; D000099152:Cadherin 5
D020533:Angiogenesis Inhibitors; D015703:Antigens, CD; D015820:Cadherins; D015815:Cell Adhesion Molecules; D007136:Immunoglobulins; D018836:Inflammation Mediators; D039564:Integrin alphaV; D018799:Intercellular Adhesion Molecule-1; D036341:Intercellular Signaling Peptides and Proteins; D020782:Matrix Metalloproteinases; D009088:Mucoproteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D019010:Vascular Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D000099152:Cadherin 5; C504265:MADCAM1 protein, human