Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling

Nonalcoholic steatohepatitis (NASH) and dietary cholesterol are risk factors for hepatocellular carcinoma (HCC). Here, the authors utilise mouse models to show that dietary cholesterol induces NASH by deregulating genes involved in metabolism, inflammation and calcium signaling to induce NASH-HCC.

Bibliographic Details
Main Authors: Jessie Qiaoyi Liang, Narcissus Teoh, Lixia Xu, Sharon Pok, Xiangchun Li, Eagle S. H. Chu, Jonathan Chiu, Ling Dong, Evi Arfianti, W. Geoffrey Haigh, Matthew M. Yeh, George N. Ioannou, Joseph J. Y. Sung, Geoffrey Farrell, Jun Yu
Format: Article
Language:English
Published: Nature Portfolio 2018-10-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-06931-6
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author Jessie Qiaoyi Liang
Narcissus Teoh
Lixia Xu
Sharon Pok
Xiangchun Li
Eagle S. H. Chu
Jonathan Chiu
Ling Dong
Evi Arfianti
W. Geoffrey Haigh
Matthew M. Yeh
George N. Ioannou
Joseph J. Y. Sung
Geoffrey Farrell
Jun Yu
author_facet Jessie Qiaoyi Liang
Narcissus Teoh
Lixia Xu
Sharon Pok
Xiangchun Li
Eagle S. H. Chu
Jonathan Chiu
Ling Dong
Evi Arfianti
W. Geoffrey Haigh
Matthew M. Yeh
George N. Ioannou
Joseph J. Y. Sung
Geoffrey Farrell
Jun Yu
author_sort Jessie Qiaoyi Liang
collection DOAJ
description Nonalcoholic steatohepatitis (NASH) and dietary cholesterol are risk factors for hepatocellular carcinoma (HCC). Here, the authors utilise mouse models to show that dietary cholesterol induces NASH by deregulating genes involved in metabolism, inflammation and calcium signaling to induce NASH-HCC.
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spelling doaj.art-f586a8b5cf4f4dbbb56141228ef1c3be2022-12-21T23:39:05ZengNature PortfolioNature Communications2041-17232018-10-019111310.1038/s41467-018-06931-6Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signalingJessie Qiaoyi Liang0Narcissus Teoh1Lixia Xu2Sharon Pok3Xiangchun Li4Eagle S. H. Chu5Jonathan Chiu6Ling Dong7Evi Arfianti8W. Geoffrey Haigh9Matthew M. Yeh10George N. Ioannou11Joseph J. Y. Sung12Geoffrey Farrell13Jun Yu14Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongLiver Research Group, Australian National University Medical School at the Canberra HospitalDepartment of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongLiver Research Group, Australian National University Medical School at the Canberra HospitalDepartment of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongDepartment of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongDepartment of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongDepartment of Gastroenterology and Hepatology, Zhongshan Hospital of Fudan UniversityLiver Research Group, Australian National University Medical School at the Canberra HospitalDepartment of Gastroenterology and Hepatology, Veterans Affairs Puget Sound Health Care System and University of WashingtonDepartment of Pathology, University of Washington School of MedicineDepartment of Gastroenterology and Hepatology, Veterans Affairs Puget Sound Health Care System and University of WashingtonDepartment of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongLiver Research Group, Australian National University Medical School at the Canberra HospitalDepartment of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Institute of Digestive Disease and Li Ka Shing Institute of Health Sciences, CUHK Shenzhen Research Institute, The Chinese University of Hong KongNonalcoholic steatohepatitis (NASH) and dietary cholesterol are risk factors for hepatocellular carcinoma (HCC). Here, the authors utilise mouse models to show that dietary cholesterol induces NASH by deregulating genes involved in metabolism, inflammation and calcium signaling to induce NASH-HCC.https://doi.org/10.1038/s41467-018-06931-6
spellingShingle Jessie Qiaoyi Liang
Narcissus Teoh
Lixia Xu
Sharon Pok
Xiangchun Li
Eagle S. H. Chu
Jonathan Chiu
Ling Dong
Evi Arfianti
W. Geoffrey Haigh
Matthew M. Yeh
George N. Ioannou
Joseph J. Y. Sung
Geoffrey Farrell
Jun Yu
Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
Nature Communications
title Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
title_full Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
title_fullStr Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
title_full_unstemmed Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
title_short Dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
title_sort dietary cholesterol promotes steatohepatitis related hepatocellular carcinoma through dysregulated metabolism and calcium signaling
url https://doi.org/10.1038/s41467-018-06931-6
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