Fig. 1

Endothelial adaptation to the inflammatory environment and related vascular disorders. Variety of stressors can elicit shedding of intercellular junctions in ECs (left). Loss of junctional integrity leads to recruitment of the leukocytes into the subendothelial spaces. While this adaptive event is required for the host defense and tissue maintenance, prolonged and excessive inflammatory responses cause failure of adaptation, thereby inducing fibrogenic responses in adjacent microenvironment as well as atherosclerosis and vascular dissection in large blood vessels (upper right). When ECs are subjected to the angiogenic stimuli, they migrate toward the interstitinal spaces to form new blood vessel network. Such angiogenic responses are indispensable for the tissue development and repair. However, excessive and redundant angiogenic stimuli, such as combination of growth factors and inflammatory cytokines, lead to aberrant angiogenic regulations, leading to the pathological angiogenesis, such as tumor angiogenesis and retinopathy (lower right). ANG-2: angiopoietin-2; EC: endothelial cell; FGF: fibroblast growth factor; IL-1β: interleukin-1β; IL-6: interleukin-6; TGF-β1: transforming growth factor-β1; TNF-α: tumor necrosis factor-α; VEGF: vascular endothelial growth factor