Apoptosis and angiogenesis: an evolving mechanism for fibrosis

被引:196
作者
Johnson, Ariel [1 ]
DiPietro, Luisa Ann [1 ]
机构
[1] Univ Illinois, Ctr Wound Healing & Tissue Regenerat, Chicago, IL 60612 USA
基金
美国国家卫生研究院;
关键词
wound healing; scar formation; liver; lung; allograft vasculopathy; HEPATIC STELLATE CELLS; IDIOPATHIC PULMONARY-FIBROSIS; GROWTH-FACTOR; ENDOTHELIAL-CELLS; LIVER FIBROSIS; SCAR FORMATION; LUNG FIBROSIS; EXPRESSION; TISSUE; MYOFIBROBLASTS;
D O I
10.1096/fj.12-214189
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Fibrosis, seen in the liver, lung, heart, kidney, and skin, is a significant global disease burden. Currently, therapeutic treatment is limited, and the number of cases continues to grow. Apoptosis has been identified as a potential initiator and propagator of fibrosis. This review specifically examines the correlation between the presence of apoptotic cells and their effect on fibroblast phenotype and collagen metabolism in several different experimental models of fibrosis. Fibrosis in these models is generally preceded by robust angiogenesis and vascular regression, suggesting that the vascular apoptotic burden may be important to fibrotic outcomes. This review considers the emerging evidence that angiogenesis or vascular regression contributes to fibrosis and identifies initial vascular outgrowth or vascular apoptotic cell presence as possible regulators of fibrosis. A further understanding of the cellular mechanisms of fibrosis may suggest novel methods for the reduction of the fibrotic response and promotion of regeneration.Johnson, A., DiPietro, L. A. Apoptosis and angiogenesis: an evolving mechanism for fibrosis.
引用
收藏
页码:3893 / 3901
页数:9
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