Angiogenesis and chronic inflammation: cause or consequence?

Abstract

Evidence has been gathered regarding the association between angiogenesis and inflammation in pathological situations. These two phenomena have long been coupled together in many chronic inflammatory disorders with distinct etiopathogenic origin, including psoriasis, rheumatoid arthritis, Crohn's disease, diabetes, and cancer. Lately, this concept has further been substantiated by the finding that several previously established non-inflammatory disorders, such as osteoarthritis and obesity, display both inflammation and angiogenesis in an exacerbated manner. In addition, the interplay between inflammatory cells, endothelial cells and fibroblasts in chronic inflammation sites, together with the fact that inflammation and angiogenesis can actually be triggered by the same molecular events, further strengthen this association. Therefore, elucidating the underlying cellular and molecular mechanisms that gather together the two processes is mandatory in order to understand their synergistic effect, and to develop new therapeutic approaches for the management of these disorders that cause a great deal of discomfort, disability, and in some cases death.

Dysphagia, dystussia, and aspiration pneumonia in elderly people

“…Inflammatory cells secrete many angiogenic and lymphangiogenic factors, including VEGF families, TNFα, and other cytokines (22,23). Multiple types of leukocytes and macrophages contribute to proteolytic remodeling of the extracellular matrix (24,25).…”

“…Multiple types of leukocytes and macrophages contribute to proteolytic remodeling of the extracellular matrix (24,25). Angiogenesis and lymphangiogenesis facilitate additional recruitment of immune cells, resulting in enhancement of chronic inflammation (23,25,26). On the other hand, elevated levels of inflammatory cytokines such as TNFα, IL-1, and IL-6 induce a decrease in muscle mass and strength, called sarcopenia (27)(28)(29)(30).…”

Angiopoietin/Tie2 Signaling Transforms Capillaries into Venules Primed for Leukocyte Trafficking in Airway Inflammation

“…3 In acute inflammation, plasma leakage and leukocyte migration are restricted to venules, but in chronic inflammation the responsive region of the microvasculature expands by transformation of capillaries into a venular phenotype. 4,5 Although the remodeled vessels have been considered enlarged, dilated, or engorged capillaries because of their location and size, they have features of venules and thereby contribute to the gatekeeper role of venules in controlling plasma extravasation and leukocyte infiltration. 5 Such remodeled vessels are seen in the airways of asthmatics, 6 skin lesion of psoriasis, 7 and intestine of inflammatory bowel disease.…”

Role of Inflammation and Angiogenic Growth Factors in Malignant Mesothelioma

“…The high amount of chemokines/cytokines, growth factors, proteolytic enzymes, proteoglycans, lipid mediators and prostaglandins which is typically found in the tumor microenvironment sustains and exacerbates both inflammation and angiogenesis (Costa et al, 2007;Lin & Karin, 2007;Ono, 2008). In this context, the cross-talk between inflammation and angiogenesis is further corroborated by the evidence that, if on one hand inflammatory mediators have significant effects on angiogenesis, on the other hand angiogenic factors can effectively promote inflammation.…”