Mesenchymal cell proliferation and programmed cell death: key players in fibrogenesis and new targets for therapeutic intervention

被引:13
作者
Luna, Jeroni [1 ]
Carme Masamunt, Maria [1 ]
Lawrance, Ian Craig [2 ]
Sans, Miquel [1 ]
机构
[1] Hosp Clin Barcelona, IDIBAPS, CIBER EHD, Dept Gastroenterol, Barcelona 08036, Catalunya, Spain
[2] Univ Western Australia, Sch Med & Pharmacol, Fremantle, WA, Australia
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2011年 / 300卷 / 05期
关键词
inflammatory bowel disease; Crohn's disease; HEPATIC STELLATE CELLS; FRACTALKINE RECEPTOR CX3CR1; HEPATOCYTE GROWTH-FACTOR; GENOME-WIDE ASSOCIATION; CROHNS-DISEASE; GENE-EXPRESSION; LIVER FIBROSIS; RETINOIC ACID; FIBROSTENOSING DISEASE; PULMONARY-FIBROSIS;
D O I
10.1152/ajpgi.00504.2010
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
An exquisite equilibrium between cell proliferation and programmed cell death is required to maintain physiological homeostasis. In inflammatory bowel disease, and especially in Crohn's disease, enhanced proliferation along with defective apoptosis of immune cells are considered key elements of pathogenesis. Despite the relatively limited attention that has been given to research efforts devoted to intestinal fibrosis to date, there is evidence suggesting that enhanced proliferation along with defective programmed cell death of mesenchymal cells can significantly contribute to the development of excessive fibrogenesis in many different tissues. Moreover, some therapies have demonstrated potential antifibrogenic efficacy through the regulation of mesenchymal cell proliferation and programmed cell death. Further understanding of the pathways involved in the regulation of mesenchymal cell proliferation and apoptosis is, however, required.
引用
收藏
页码:G703 / G708
页数:6
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