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Fibrogenesis of Parenchymal Organs

¹ Department of Medicine, University of California, San Diego, La Jolla, California

Correspondence and requests for reprints should be addressed to David Brenner, M.D., 1318A Biomedical Sciences Building, 9500 Gilman Drive, La Jolla, CA 92093-0602. E-mail: dbrenner{at}ucsd.edu

ABSTRACT

Fibrosis of parenchymal organs is caused by prolonged injury, deregulation of the normal processes of wound healing, and extensive deposition of extracellular matrix (ECM) proteins. The current review will focus on common features of fibrogenesis in parenchymal organs, and will briefly discuss common features and differences in the pathophysiology of fibrosis. Comparison of hepatic, renal, and pulmonary fibrosis has identified several common mechanisms. Common themes include a critical role for the cytokine transforming growth factor β and the generation of reactive oxygen species. Activated myofibroblasts are the common cell type that produce the excessive fibrous scar and may originate from endogenous cells such as hepatic stellate cells or fibroblasts, from the bone marrow such as fibrocytes, or from the transition of epithelial cells to mesenchymal cells. These concepts open new prospects for multidisciplinary research and the development of new therapies for fibrosis.

Key Words: fibrosis • collagen type I • inflammation • EMT