Angiogenesis in inflammatory bowel disease

Abstract

Both ulcerative colitis and Crohn's disease, the two major forms of inflammatory bowel diseases, are recognized, at the moment, as perplexing and challenging clinical entities, in which several molecules and cell types are implicated. Recent molecular evidence proposes the intestinal microvascular remodelling or angiogenesis, as a phenomenon implicated in the pathogenesis of these chronic inflammatory disorders, together with other proposed theories involved in the pathogenesis of inflammatory bowel diseases, such as genetic, microbacterial and immune factors.Intestinal damage is followed by a physiological angiogenesis, but the abnormal expression of pro-and anti-angiogenic molecules and the changes of vascular cell types could reflect a pathological vascular remodelling. Thus, the inflammation may be favoured and maintained by a pathological angiogenesis.A better understanding of the angiogenic process may facilitate the design of more effective therapies for chronic intestinal inflammation.

Clotrimazole Ameliorates Intestinal Inflammation and Abnormal Angiogenesis by Inhibiting Interleukin-8 Expression through a Nuclear Factor-κB-Dependent Manner

“…Several lines of evidence have implicated that the pathogenesis of chronic inflammatory disease, including IBD, involves angiogenesis (Pousa et al, 2008). Based on these notions, the antiangiogenic approach is suggested as a new therapeutic intervention for chronic inflammatory diseases (Danese et al, 2007).…”

The Gastrointestinal Circulation: Physiology and Pathophysiology

“…The colon is a major target organ for chronic inflammatory diseases, most notably ulcerative colitis (UC) and Crohn's disease (CD). While the etiology of the inflammatory bowel diseases (IBD) remains poorly understood, there has been growing interest in defining the role of the colonic vasculature in the initiation, perpetuation, and regulation of inflammation in this tissue (198,226,394). It is now recognized that the inflamed colonic microvasculature exhibits different functional and structural changes that are manifested in all segments of the vascular tree, including arterioles, capillaries and venules (302).…”

Corticosteroids Modulate Angiogenic Soluble Factors in Ulcerative Colitis Patients

“…Angiogenesis has emerged as a vascular mechanism contributing to chronic inflammation in inflammatory bowel disease [6,16,32]. Since VEGF/PlGF-VEGFR1 and Ang1/Ang2-Tie2 systems have been thought to play a major role in the regulation of most phases of the neovascularization process [17,33], inhibition of its circulating levels could be a potential therapeutic approach in preventing intestinal mucosa damage and the perpetuation of the gut inflammation.…”

“…Increasing evidence supports the role of angiogenesis, not only in neoplastic disorders, but also in a diverse range of non-neoplastic inflammatory conditions such as autoimmune liver diseases, rheumatoid arthritis, diabetes retinopathy, psoriasis, atherosclerosis, and inflammatory bowel diseases [2][3][4][5][6][7][8][9][10][11]. It is well understood that chronic inflammation and angiogenesis are codependent processes [12,13].…”

“…Alterations in the strict regulation of the expression of all these factors could be crucial in developing new blood vessels from pre-existing ones, which could possibly contribute to the chronic inflammation in the gut of UC patients [6]. Overexpression of VEGF has been described in both experimental colitis [22,23] and UC patients [24][25][26], and although evidence exists that corticosteroids suppress VEGF production [27,28], not much is known about the effect of corticosteroids on the serum levels of VEGF, PlGF, VEG-FR1, Ang1, Ang2 and Tie2 in active UC.…”