Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets?

Research output: Contribution to journal › Review › Research › peer-review

Standard

Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets? / Zisser, Alexandra; Ipsen, David H; Tveden-Nyborg, Pernille.

In: Biomedicines, Vol. 9, No. 4, 365, 2021.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Zisser, A, Ipsen, DH & Tveden-Nyborg, P 2021, 'Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets?', Biomedicines, vol. 9, no. 4, 365. https://doi.org/10.3390/biomedicines9040365

APA

Zisser, A., Ipsen, D. H., & Tveden-Nyborg, P. (2021). Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets? Biomedicines, 9(4), [365]. https://doi.org/10.3390/biomedicines9040365

Vancouver

Zisser A, Ipsen DH, Tveden-Nyborg P. Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets? Biomedicines. 2021;9(4). 365. https://doi.org/10.3390/biomedicines9040365

Author

Zisser, Alexandra ; Ipsen, David H ; Tveden-Nyborg, Pernille. / Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets?. In: Biomedicines. 2021 ; Vol. 9, No. 4.

Bibtex

@article{7132f30131f24581a1b3690f3a0ebce7,
title = "Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets?",
abstract = "Hepatic fibrosis is the primary predictor of mortality in patients with non-alcoholic steatohepatitis (NASH). In this process, the activated hepatic stellate cells (HSCs) constitute the principal cells responsible for the deposition of a fibrous extracellular matrix, thereby driving the hepatic scarring. HSC activation, migration, and proliferation are controlled by a complex signaling network involving growth factors, lipotoxicity, inflammation, and cellular stress. Conversely, the clearance of activated HSCs is a prerequisite for the resolution of the extracellular fibrosis. Hence, pathways regulating the fate of the HSCs may represent attractive therapeutic targets for the treatment and prevention of NASH-associated hepatic fibrosis. However, the development of anti-fibrotic drugs for NASH patients has not yet resulted in clinically approved therapeutics, underscoring the complex biology and challenges involved when targeting the intricate cellular signaling mechanisms. This narrative review investigated the mechanisms of activation and inactivation of HSCs with a focus on NASH-associated hepatic fibrosis. Presenting an updated overview, this review highlights key cellular pathways with potential value for the development of future treatment modalities.",
author = "Alexandra Zisser and Ipsen, {David H} and Pernille Tveden-Nyborg",
year = "2021",
doi = "10.3390/biomedicines9040365",
language = "English",
volume = "9",
journal = "Biomedicines",
issn = "2227-9059",
publisher = "MDPI AG",
number = "4",

}

RIS

TY - JOUR

T1 - Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis—Roles as Putative Treatment Targets?

AU - Zisser, Alexandra

AU - Ipsen, David H

AU - Tveden-Nyborg, Pernille

PY - 2021

Y1 - 2021

N2 - Hepatic fibrosis is the primary predictor of mortality in patients with non-alcoholic steatohepatitis (NASH). In this process, the activated hepatic stellate cells (HSCs) constitute the principal cells responsible for the deposition of a fibrous extracellular matrix, thereby driving the hepatic scarring. HSC activation, migration, and proliferation are controlled by a complex signaling network involving growth factors, lipotoxicity, inflammation, and cellular stress. Conversely, the clearance of activated HSCs is a prerequisite for the resolution of the extracellular fibrosis. Hence, pathways regulating the fate of the HSCs may represent attractive therapeutic targets for the treatment and prevention of NASH-associated hepatic fibrosis. However, the development of anti-fibrotic drugs for NASH patients has not yet resulted in clinically approved therapeutics, underscoring the complex biology and challenges involved when targeting the intricate cellular signaling mechanisms. This narrative review investigated the mechanisms of activation and inactivation of HSCs with a focus on NASH-associated hepatic fibrosis. Presenting an updated overview, this review highlights key cellular pathways with potential value for the development of future treatment modalities.

AB - Hepatic fibrosis is the primary predictor of mortality in patients with non-alcoholic steatohepatitis (NASH). In this process, the activated hepatic stellate cells (HSCs) constitute the principal cells responsible for the deposition of a fibrous extracellular matrix, thereby driving the hepatic scarring. HSC activation, migration, and proliferation are controlled by a complex signaling network involving growth factors, lipotoxicity, inflammation, and cellular stress. Conversely, the clearance of activated HSCs is a prerequisite for the resolution of the extracellular fibrosis. Hence, pathways regulating the fate of the HSCs may represent attractive therapeutic targets for the treatment and prevention of NASH-associated hepatic fibrosis. However, the development of anti-fibrotic drugs for NASH patients has not yet resulted in clinically approved therapeutics, underscoring the complex biology and challenges involved when targeting the intricate cellular signaling mechanisms. This narrative review investigated the mechanisms of activation and inactivation of HSCs with a focus on NASH-associated hepatic fibrosis. Presenting an updated overview, this review highlights key cellular pathways with potential value for the development of future treatment modalities.

U2 - 10.3390/biomedicines9040365

DO - 10.3390/biomedicines9040365

M3 - Review

C2 - 33807461

VL - 9

JO - Biomedicines

JF - Biomedicines

SN - 2227-9059

IS - 4

M1 - 365

ER -

ID: 260001960