Review
Version 1
Preserved in Portico This version is not peer-reviewed
Role of Gut-Microbiota in Hepatocarcinogenesis
Version 1
: Received: 27 March 2019 / Approved: 28 March 2019 / Online: 28 March 2019 (13:43:07 CET)
A peer-reviewed article of this Preprint also exists.
Gupta, H.; Youn, G.S.; Shin, M.J.; Suk, K.T. Role of Gut Microbiota in Hepatocarcinogenesis. Microorganisms 2019, 7, 121. Gupta, H.; Youn, G.S.; Shin, M.J.; Suk, K.T. Role of Gut Microbiota in Hepatocarcinogenesis. Microorganisms 2019, 7, 121.
Abstract
Hepatocellular carcinoma (HCC), one of the leading causes of death worldwide, has a causal nexus with liver injury, inflammation, and regeneration that accumulate over decades. Observations from recent studies have accounted for the involvement of the gut-liver axis in the pathophysiological mechanism responsible for HCC. The human intestine nurtures a diversified colony of microorganisms residing in the host ecosystem. The intestinal barrier is critical for conserving the normal physiology of the gut microbiome. Therefore, a rupture of this barrier or dysbiosis cause the intestinal microbiome to serve as the main source of portal-vein endotoxins such as lipopolysaccharide, in the progression of hepatic diseases. Indeed, increased bacterial translocation is a key sign of HCC. Considering the limited number of clinical studies on HCC with respect to the microbiome, we focus on the clinical as well as animal studies involving the gut microbiota with the current understandings of the mechanism by which the intestinal dysbiosis promotes hepatocarcinogenesis. Future research might offer mechanistic insights into the specific phyla targeting the leaky gut, as well as microbial dysbiosis, and their metabolites, as key pathways that drive HCC-promoting microbiome-mediated liver inflammation and fibrosis, thereby restoring the gut barrier function.
Keywords
hepatocellular carcinoma, gut microbiota, gut-liver axis, intestinal dysbiosis
Subject
Medicine and Pharmacology, Gastroenterology and Hepatology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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