2015
DOI: 10.1007/s12020-015-0803-7
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Periostin on the road to nonalcoholic fatty liver disease

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Cited by 5 publications
(2 citation statements)
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“…Besides steatosis, PN has been demonstrated to mediate also hepatic inflammation and fibrosis, probably through both direct and indirect mechanisms related to the concomitant release of pro-inflammatory and pro-fibrotic factors and inhibition of adiponectin, an insulin-sensitizing and anti-inflammatory adipokine. Despite this experimental evidence, there are currently limited data for PN in human NAFLD evolved to NASH or hepatic fibrosis/cirrhosis (which could be expected to present higher PN levels than SS patients) [8,20].…”
Section: Introductionmentioning
confidence: 99%
“…Besides steatosis, PN has been demonstrated to mediate also hepatic inflammation and fibrosis, probably through both direct and indirect mechanisms related to the concomitant release of pro-inflammatory and pro-fibrotic factors and inhibition of adiponectin, an insulin-sensitizing and anti-inflammatory adipokine. Despite this experimental evidence, there are currently limited data for PN in human NAFLD evolved to NASH or hepatic fibrosis/cirrhosis (which could be expected to present higher PN levels than SS patients) [8,20].…”
Section: Introductionmentioning
confidence: 99%
“…To the best of our knowledge, JPD due to homozygosity for the TNFRSF11B "Balkan mutation" (966_969delTGACinsCTT), resulting in non-functioning osteoprotegerin, has been described in only five patients todate (5). Periostin, a secreted extracellular matrix protein, is expressed in collagen rich connective tissues and interacts with several cell surface integrins, providing signals for tissue development and remodeling (6). Sclerostin, produced almost exclusively by the osteocytes, is a negative regulator of the canonical Wingless (Wnt)/β-catenin signaling, thus inhibiting osteoblastic bone formation (7).…”
Section: Introductionmentioning
confidence: 99%