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Review
. 2022 Dec 6:10:e14299.
doi: 10.7717/peerj.14299. eCollection 2022.

Hypoxia-induced factor and its role in liver fibrosis

Affiliations
Review

Hypoxia-induced factor and its role in liver fibrosis

Jan Mohammad Omar et al. PeerJ. .

Abstract

Liver fibrosis develops as a result of severe liver damage and is considered a major clinical concern throughout the world. Many factors are crucial for liver fibrosis progression. While advancements have been made to understand this disease, no effective pharmacological drug and treatment strategies have been established that can effectively prevent liver fibrosis or even could halt the fibrotic process. Most of those advances in curing liver fibrosis have been aimed towards mitigating the causes of fibrosis, including the development of potent antivirals to inhibit the hepatitis virus. It is not practicable for many individuals; however, a liver transplant becomes the only suitable alternative. A liver transplant is an expensive procedure. Thus, there is a significant need to identify potential targets of liver fibrosis and the development of such agents that can effectively treat or reverse liver fibrosis by targeting them. Researchers have identified hypoxia-inducible factors (HIFs) in the last 16 years as important transcription factors driving several facets of liver fibrosis, making them possible therapeutic targets. The latest knowledge on HIFs and their possible role in liver fibrosis, along with the cell-specific activities of such transcription factors that how they play role in liver fibrosis progression, is discussed in this review.

Keywords: Alcoholic fatty liver disease; Fatty liver diseases; Hepatocellular carcinoma; Hyoxia-induced factors; Hyptocytes; Kapffur cells; Liver cirrhosis; Liver fibrosis; Macrophages; Stellate cells.

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Conflict of interest statement

The authors declare there are no competing interests.

Figures

Figure 1
Figure 1. (A) Regulation of HIF in normal conditions (normoxia), (B) regulation of HIF in hypoxia conditions.
Figure 2
Figure 2. Regulation of HIF independent of oxygen.
Figure 3
Figure 3. Pro-fibrotic function of HIFs in liver fibrosis.

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