- 作者: Tien Hsu, Hieu-Huy Nguyen-Tran and Maria Trojanowska
- 作者服務機構: 1. Department of Biomedical Sciences and Engineering, National Central University, 300 Jhongda Rd, Taoyuan City, Taiwan, Republic of China 2. Center for Chronic Disease Research, National Central University, 300 Jhongda Rd, Taoyuan City, Taiwan, Republic of China 3. Arthritis Center, Boston University School of Medicine, 75 E. Newton St. Evans Building, Boston, MA, 02118, USA
- 中文摘要:
- 英文摘要:
Chronic inflammation is the underlying pathological condition that results in fibrotic diseases. More recently, many forms of cancer have also been linked to chronic tissue inflammation. While stromal immune cells and myofibroblasts have been recognized as major contributors of cytokines and growth factors that foster the formation of fibrotic tissue, the endothelium has traditionally been regarded as a passive player in the pathogenic process, or even as a barrier since it provides a physical divide between the circulating immune cells and the inflamed tissues. Recent findings, however, have indicated that endothelial cells in fact play a crucial role in the inflammatory response. Endothelial cells can be activated by cytokine signaling and express inflammatory markers, which can sustain or exacerbate the inflammatory process. For example, the activated endothelium can recruit and activate leukocytes, thus perpetuating tissue inflammation, while sustained stimulation of endothelial cells may lead to endothelial-to-mesenchymal transition that contributes to fibrosis. Since chronic inflammation has now been recognized as a significant contributing factor to tumorigenesis, it has also emerged that activation of endothelium also occurs in the tumor microenvironment. This review summarizes recent findings characterizing the molecular and cellular changes in the vascular endothelium that contribute to tissue fibrosis, and potentially to cancer formation. - 中文關鍵字:
- 英文關鍵字: Inflammation, Endothelial cells, Fibrosis, Cancer vasculature