Next Article in Journal
Promising Prognosis Marker Candidates on the Status of Epithelial–Mesenchymal Transition and Glioma Stem Cells in Glioblastoma
Next Article in Special Issue
The Role of Gut-Derived Microbial Antigens on Liver Fibrosis Initiation and Progression
Previous Article in Journal
Vpr and Its Cellular Interaction Partners: R We There Yet?
Previous Article in Special Issue
MicroRNA-29a Suppresses CD36 to Ameliorate High Fat Diet-Induced Steatohepatitis and Liver Fibrosis in Mice
Open AccessReview

Roles of the Hepatic Endocannabinoid and Apelin Systems in the Pathogenesis of Liver Fibrosis

1
Biochemistry and Molecular Genetics Service, Hospital Clínic Universitari, IDIBAPS, CIBERehd, Villarroel 170, 08036 Barcelona, Spain
2
Department of Biomedicine, University of Barcelona, 08036 Barcelona, Spain
3
Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
*
Author to whom correspondence should be addressed.
Cells 2019, 8(11), 1311; https://doi.org/10.3390/cells8111311
Received: 25 September 2019 / Revised: 17 October 2019 / Accepted: 23 October 2019 / Published: 24 October 2019
Hepatic fibrosis is the consequence of an unresolved wound healing process in response to chronic liver injury and involves multiple cell types and molecular mechanisms. The hepatic endocannabinoid and apelin systems are two signalling pathways with a substantial role in the liver fibrosis pathophysiology—both are upregulated in patients with advanced liver disease. Endogenous cannabinoids are lipid-signalling molecules derived from arachidonic acid involved in the pathogenesis of cardiovascular dysfunction, portal hypertension, liver fibrosis, and other processes associated with hepatic disease through their interactions with the CB1 and CB2 receptors. Apelin is a peptide that participates in cardiovascular and renal functions, inflammation, angiogenesis, and hepatic fibrosis through its interaction with the APJ receptor. The endocannabinoid and apelin systems are two of the multiple cell-signalling pathways involved in the transformation of quiescent hepatic stellate cells into myofibroblast like cells, the main matrix-producing cells in liver fibrosis. The mechanisms underlying the control of hepatic stellate cell activity are coincident despite the marked dissimilarities between the endocannabinoid and apelin signalling pathways. This review discusses the current understanding of the molecular and cellular mechanisms by which the hepatic endocannabinoid and apelin systems play a significant role in the pathophysiology of liver fibrosis. View Full-Text
Keywords: endocannabinoids; apelin; liver fibrosis; CB1; CB2; APJ endocannabinoids; apelin; liver fibrosis; CB1; CB2; APJ
Show Figures

Figure 1

MDPI and ACS Style

Melgar-Lesmes, P.; Perramon, M.; Jiménez, W. Roles of the Hepatic Endocannabinoid and Apelin Systems in the Pathogenesis of Liver Fibrosis. Cells 2019, 8, 1311.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop