A New Molecular Target for Blunting Organ Fibrosis. Focus On "Secreted Frizzled-Related Protein 2 (SFRP2) As a Target in Anti-Fibrotic Therapeutic Intervention"

Document Type

Article

Publication Date

2014

Abstract

"Fribrosis is a pathology associated with failure of many different organs, including the heart, lung, kidney, liver, and the vasculature. Fibrosis results from wound healing (and in some cases developmental) processes that become prolonged or dysregulated. Following tissue damage, inflammation at the site of injury produces a gush of cytokines that signal subsequent myofibroblast differentiation and cell proliferation, wound closure and neovascularization, and then tissue matrix deposition that form a fibrous scar. The final step, which accompanies the return to normal tissue function, involves senescence or death of the activated myofibroblasts, which mediate the extracellular matrix (ECM) production, to return to normal organ function (7). Prolonged activation (i.e., inflammation and cytokine production) of these wound healing processes or loss of negative feedback loops that terminate these processes likely underlie the development of pathological fibrosis."

Comments

This article was originally published in American Journal of Physiology - Cell Physiology, volume 306, issue 6, in 2014. DOI: 10.1152/ajpcell.00020.2014

Copyright

American Physiological Society

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