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Cellular and molecular mechanisms of intestinal fibrosis

World Journal of Gastroenterology 2012年第28期18卷 3635-3661页

作者： Silvia Speca Ilaria Giusti Florian Rieder Giovanni Latella Gastroenterology Unit Department of Internal Medicine and Public Health University of L'Aquila 67100 L'Aquila Italy Department of Gastroenterology and Hepatology Lerner Research Institute Cleveland Clinic Foundation Cleveland OH 73051 United States

Fibrosis is a chronic and progressive process characterized by an excessive accumulation of extracellular matrix (ECM) leading to stiffening and/or scarring of the involved tissue. Intestinal fibrosis may develop in several different enteropathies, including inflammatory bowel disease. It develops through complex cell, extracellular matrix, cytokine and growth factor interactions. Distinct cell types are involved in intestinal fibrosis, such as resident mesenchymal cells (fibroblasts, myofibroblasts and smooth muscle cells) but also ECM-producing cells derived from epithelial and endothelial cells (through a process termed epithelialand endothelial-mesenchymal transition), stellate cells, pericytes, local or bone marrow-derived stem cells. The most important soluble factors that regulate the activation of these cells include cytokines, chemokines, growth factors, components of the renin-angiotensin system, angiogenic factors, peroxisome proliferator-activated receptors, mammalian target of rapamycin, and products of oxidative stress. It soon becomes clear that although inflammation is responsible for triggering the onset of the fibrotic proc-ess, it only plays a minor role in the progression of this condition, as fibrosis may advance in a self-perpetuating fashion. Definition of the cellular and molecular mechanisms involved in intestinal fibrosis may provide the key to developing new therapeutic approaches.

关键词： Inflammatory bowel disease Intestinal fibrosis Extracellular matrix molecular mediators Myofibroblasts Inflammatory cells Epithelial cells Mesenchymal cells Endothelial cells

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