Next Article in Journal
Determination of Homoarginine, Arginine, NMMA, ADMA, and SDMA in Biological Samples by HPLC-ESI-Mass Spectrometry
Next Article in Special Issue
Combined Taurine, Epigallocatechin Gallate and Genistein Therapy Reduces HSC-T6 Cell Proliferation and Modulates the Expression of Fibrogenic Factors
Previous Article in Journal
Disease Animal Models of TDP-43 Proteinopathy and Their Pre-Clinical Applications
Previous Article in Special Issue
Immunological Mechanisms in the Pathophysiology of Non-Alcoholic Steatohepatitis
 
 
Review

Role of Hepatic Progenitor Cells in Nonalcoholic Fatty Liver Disease Development: Cellular Cross-Talks and Molecular Networks

1
Department of Anatomical, Histological, Forensic Medicine and Orthopedics Sciences, Sapienza University of Rome, Rome 00161, Italy
2
Department of Movement, Human and Health Sciences, University of Rome "Foro Italico", Piazza Lauro De Bosis 6, Rome 00135, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2013, 14(10), 20112-20130; https://doi.org/10.3390/ijms141020112
Received: 6 August 2013 / Revised: 18 September 2013 / Accepted: 18 September 2013 / Published: 9 October 2013
(This article belongs to the Special Issue Non-Alcoholic Fatty Liver Disease Research)
Nonalcoholic fatty liver disease (NAFLD) includes a spectrum of diseases ranging from simple fatty liver to nonalcoholic steatohepatitis, (NASH) which may progress to cirrhosis and hepatocellular carcinoma. NASH has been independently correlated with atherosclerosis progression and cardiovascular risk. NASH development is characterized by intricate interactions between resident and recruited cells that enable liver damage progression. The increasing general agreement is that the cross-talk between hepatocytes, hepatic stellate cells (HSCs) and macrophages in NAFLD has a main role in the derangement of lipid homeostasis, insulin resistance, danger recognition, immune tolerance response and fibrogenesis. Moreover, several evidences have suggested that hepatic stem/progenitor cell (HPCs) activation is a component of the adaptive response of the liver to oxidative stress in NAFLD. HPC activation determines the appearance of a ductular reaction. In NASH, ductular reaction is independently correlated with progressive portal fibrosis raising the possibility of a periportal fibrogenetic pathway for fibrogenesis that is parallel to the deposition of subsinusoidal collagen in zone 3 by HSCs. Recent evidences indicated that adipokines, a class of circulating factors, have a key role in the cross-talk among HSCs, HPCs and liver macrophages. This review will be focused on cellular cross-talk and the relative molecular networks which are at the base of NASH progression and fibrosis. View Full-Text
Keywords: nonalcoholic fatty liver disease; hepatic progenitor cell; hepatic stellate cells; macrophages; kupffer cells; fibrogenesis nonalcoholic fatty liver disease; hepatic progenitor cell; hepatic stellate cells; macrophages; kupffer cells; fibrogenesis
Show Figures

Graphical abstract

MDPI and ACS Style

Carpino, G.; Renzi, A.; Onori, P.; Gaudio, E. Role of Hepatic Progenitor Cells in Nonalcoholic Fatty Liver Disease Development: Cellular Cross-Talks and Molecular Networks. Int. J. Mol. Sci. 2013, 14, 20112-20130. https://doi.org/10.3390/ijms141020112

AMA Style

Carpino G, Renzi A, Onori P, Gaudio E. Role of Hepatic Progenitor Cells in Nonalcoholic Fatty Liver Disease Development: Cellular Cross-Talks and Molecular Networks. International Journal of Molecular Sciences. 2013; 14(10):20112-20130. https://doi.org/10.3390/ijms141020112

Chicago/Turabian Style

Carpino, Guido, Anastasia Renzi, Paolo Onori, and Eugenio Gaudio. 2013. "Role of Hepatic Progenitor Cells in Nonalcoholic Fatty Liver Disease Development: Cellular Cross-Talks and Molecular Networks" International Journal of Molecular Sciences 14, no. 10: 20112-20130. https://doi.org/10.3390/ijms141020112

Find Other Styles

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Back to TopTop