Retinol dehydrogenase 13 deficiency diminishes carbon tetrachloride-induced liver fibrosis in mice.

Toxicol Lett

State Key Laboratory of Medical Genomics, Research Center for Experimental Medicine, Shanghai Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, 200025, China; Model Organism Division, E-Institutes of Shanghai Jiao Tong Universities School of Medicine (SJTUSM), Shanghai, 200025, China; Shanghai Research Center for Model Organisms, Shanghai, 201203, China. Electronic address:

Published: January 2017

Retinol dehydrogenase 13 (RDH13) is a mitochondrion-localized member of the short-chain dehydrogenases/reductases (SDRs) superfamily that participates in metabolism of some compounds. Rdh13 mRNA is most highly expressed in mouse liver. Rdh13 deficiency reduces the extent of liver injury and fibrosis, reduces hepatic stellate cell (HSC) activation, attenuates collagen I (II), tissue inhibitor of metalloproteinase 1 (TIMP-1) and transforming growth factor beta 1 (Tgf-β1) expression. The results indicate an important role of Rdh13 and suggest RDH13 as a possible new therapeutic target for CCl-induced fibrosis.

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http://dx.doi.org/10.1016/j.toxlet.2016.11.010DOI Listing

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