Preprint Review Version 1 This version is not peer-reviewed

The Cellular Pathways of Liver Fibrosis in NASH

Version 1 : Received: 23 October 2019 / Approved: 24 October 2019 / Online: 24 October 2019 (15:48:02 CEST)

How to cite: Méndez-Sánchez, N.; Coronel-Castillo, C.E.; Contreras-Carmona, J.; Barranco-Fragoso, B.; Qi, X. The Cellular Pathways of Liver Fibrosis in NASH. Preprints 2019, 2019100282 (doi: 10.20944/preprints201910.0282.v1). Méndez-Sánchez, N.; Coronel-Castillo, C.E.; Contreras-Carmona, J.; Barranco-Fragoso, B.; Qi, X. The Cellular Pathways of Liver Fibrosis in NASH. Preprints 2019, 2019100282 (doi: 10.20944/preprints201910.0282.v1).

Abstract

Nonalcoholic steatohepatitis (NASH), which is characterized by liver steatosis, inflammation and fibrosis, is the most severe variation of nonalcoholic fatty liver disease (NAFLD). This disease is a consequence of several metabolic alterations such as type 2 diabetes and dyslipidemia that trigger different pathways of cell dysfunction and systemic inflammation which ultimately affect the liver. Furthermore, those mechanisms activate a complex cascade of immune response after repeated cell aggression. In the liver cytokines and interleukins interact with network of innate immune cells, including Kupffer cells (KCs), dendritic cells (DCs), lymphocytes and hepatic stellate cells (HSC). These cells translate those signals into immune responses and pathologic hepatic changes during the development of NASH. In this scenario the development of fibrosis is the most important change since it is an adaptive mechanism that in the short time has the objective of repair the damaged tissue but after prolonged injury it progresses to parenchymal scarring, cellular dysfunction and finally to organ failure. Finally, since NASH is an important cause of liver cirrhosis; this review addresses the cellular pathways of fibrosis in the setting of NASH explained by the interaction between immune and hepatic cells.

Subject Areas

liver fibrosis; NASH; innate immune cells.

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our diversity statement.

Leave a public comment
Send a private comment to the author(s)
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.