Publication: Adiponectin as a novel biomarker for liver fibrosis
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Issued Date
2018-10-01
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ISSN
19485182
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2-s2.0-85055706392
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Mahidol University
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SCOPUS
Bibliographic Citation
World Journal of Hepatology. Vol.27, No.10 (2018), 708-718
Suggested Citation
Wanvisa Udomsinprasert, Sittisak Honsawek, Yong Poovorawan Adiponectin as a novel biomarker for liver fibrosis. World Journal of Hepatology. Vol.27, No.10 (2018), 708-718. doi:10.4254/wjh.v10.i10.708 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/46280
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Title
Adiponectin as a novel biomarker for liver fibrosis
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Abstract
© The Author(s) 2018. Adiponectin is known to play primary roles in the regulation of systemic glucose homeostasis and lipid metabolism. Interestingly, emerging evidence indicates beneficial effects of adiponectin on liver fibrosis; however, the exact mechanisms of this action remain unclear. Herein, we aimed to summarize the recent findings regarding the role of adiponectin in liver fibrogenesis and update the current comprehensive knowledge regarding usefulness of adiponectin-based treatments in liver fibrosis. Adiponectin has been demonstrated to have an anti-fibrotic action in the liver by blocking the activation of hepatic stellate cellmediated adenosine monophosphate-activated protein kinase and peroxisome proliferator-activated receptoralpha pathways, which in turn diminish the expression of pro-fibrotic genes. In addition, hyperadiponectinemia was noted in patients with various chronic liver diseases (CLDs)-related liver fibrosis. An increase in circulating adiponectin levels was also found to be associated with the development of liver fibrosis, indicating a role of adiponectin as a non-invasive biomarker for predicting the progression of liver fibrosis. It is therefore reasonable to speculate that adiponectin may be developed as a new therapeutic candidate for the treatment of liver fibrosis. Nonetheless, future observations are still necessary to fully elucidate the extent of the effects of adiponectin on liver fibrotic outcomes, in order to modify adiponectin as an anti-fibrotic therapy that would speed up fibrosis reversal in patients with CLD.