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Metalloproteinases in liver fibrosis: current insights

Authors Zbodakova O, Chalupsky K, Tureckova J, Sedlacek R

Received 11 October 2016

Accepted for publication 15 December 2016

Published 3 February 2017 Volume 2017:4 Pages 25—35


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yoshifumi Itoh

Olga Zbodakova, Karel Chalupsky, Jolana Tureckova, Radislav Sedlacek

Laboratory of Transgenic Models of Diseases, Division BIOCEV, Institute of Molecular Genetics of the ASCR, v. v. i., Prague, Czech Republic

Abstract: Liver fibrosis is defined by excessive deposition of extracellular matrix. The fibrotic conditions result from the imbalance between synthesis and deposition of fibrous tissues and decomposition of these matrix proteins. This process can be reversed as a regular part of the healing process after hepatic damage or can become chronic. When the protein matrix synthesis predominates and the decomposition is suppressed, fibrosis will progress into irreversible cirrhosis or steatosis. Among the molecular players involved in fibrotic liver diseases, metalloproteinases of matrix metalloproteinase (MMP) and a disintegrin and metalloproteinase (ADAM) families are critical in the development of liver fibrosis and its resolution. Previously, MMPs were recognized as extracellular matrix degrading enzymes. Currently, they are also known as mediators in a variety of processes related to immunity and tissue repair. In this article, we have reviewed the models of liver fibrosis and findings on MMPs and ADAMs in hepatic fibrosis conditions.

Keywords: matrix metalloproteinase, ADAM, liver, fibrosis

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