NDLI: Myofibroblasts: Biochemical and proteomic approaches to fibrosis.

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Myofibroblasts: Biochemical and proteomic approaches to fibrosis.

Content Provider	Semantic Scholar
Author	Honda, Eiko Park, Alexander Yoshida, Koji Tabuchi, Masaki Munakata, Hiroshi
Copyright Year	2013
Abstract	Fibrosis is a state, in which excess amounts of extracellular matrix are deposited in the tissue. Fibrosis can occur in various organs, including the liver, lung, kidney and heart. The progression of fibrosis involves interstitial hypercellularity, accumulation of extracellular matrix, and atrophy of epithelial structures, resulting in a loss of normal function. Myofibroblasts play a crucial role in the development and progress of fibrosis. When stimulated, myofibroblasts actively synthesize connective tissue components and cause organ fibrosis. As a result, the process and the mechanism of myofibroblast activation represent a target for antifibrotic treatment. As yet, however, an effective treatment has not been developed, and new treatment modalities are expected. Because activation of myofibroblasts is a key event during fibrosis development, there is great interest in identifying and characterizing proteins whose expression is changed after this activation. In this review, fibrosis is outlined and the role of myofibroblasts in this disorder is described. Furthermore, the search for candidate proteins to target for treatment and the prospects of antifibrotic therapy are discussed.
Starting Page	67
Ending Page	73
Page Count	7
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.journal.med.tohoku.ac.jp/2302/230_67.pdf
PubMed reference number	23774326v1
Volume Number	230
Issue Number	2
Journal	The Tohoku journal of experimental medicine
Language	English
Access Restriction	Open
Subject Keyword	Atrophic Connective Tissue Extracellular Matrix Fibrosis Hyperplasia Kidney Diseases Liver diseases Myofibroblasts Organ Pneumonia Pneumonia, Interstitial Renal Tissue Structure of parenchyma of lung Therapeutic procedure
Content Type	Text
Resource Type	Article

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