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Review
. 2021 Dec 3:12:767314.
doi: 10.3389/fendo.2021.767314. eCollection 2021.

Current and Potential Therapies Targeting Inflammation in NASH

Affiliations
Review

Current and Potential Therapies Targeting Inflammation in NASH

Somaya Albhaisi et al. Front Endocrinol (Lausanne). .

Abstract

Nonalcoholic steatohepatitis (NASH) is the advanced form of nonalcoholic fatty liver disease (NAFLD). It is characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis. Inflammation plays a key role in the progression of NASH and can be provoked by intrahepatic (e.g., lipotoxicity, immune responses, oxidative stress and cell death) and extrahepatic sources (adipose tissue or gut). The identification of triggers of inflammation is central to understanding the mechanisms in NASH development and progression and in designing targeted therapies that can halt or reverse the disease. In this review, we summarize the current and potential therapies targeting inflammation in NASH.

Keywords: cytokines; hepatocellular injury; inflammation; lymphocytes; macrophages; non-alcoholic steatohepatitis; oxidative stress; treatment.

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Conflict of interest statement

MN has been on the advisory board for 89BIO, Gilead, Intercept, Pfizer, Novo Nordisk, Blade, EchoSens, Fractyl, Terns, Siemens and Roche diagnostic; MN has received research support from Allergan, BMS, Gilead, Galmed, Galectin, Genfit, Conatus, Enanta, Madrigal, Novartis, Shire, Viking and Zydus; MN is a minor shareholder or has stocks in Anaetos, Rivus Pharma and Viking. The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Inflammation associated with NASH. Inflammation is driven by the cellular interplay involving hepatocytes, hepatic stellate cells and recruited immune cells. Hepatocyte death and inflammatory mediators are key contributors to inflammation in NAFLD and NASH progression. ILC, innate lymphoid cells; LSECs, liver sinusoidal endothelial cells; MCP-1, macrophage chemotactic protein 1; MPO, myeloperoxidase.

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