Ghrelin regulating liver activity and its potential effects on liver fibrosis and Echinococcosis

Jiang Zhu; Tanfang Zhou; Meng Menggen; Kalibixiati Aimulajiang; Hao Wen

doi:10.3389/fcimb.2023.1324134

Ghrelin regulating liver activity and its potential effects on liver fibrosis and Echinococcosis

Front Cell Infect Microbiol. 2024 Jan 8:13:1324134. doi: 10.3389/fcimb.2023.1324134. eCollection 2023.

Authors

Jiang Zhu^{1

2}, Tanfang Zhou^{1

2}, Meng Menggen¹, Kalibixiati Aimulajiang¹, Hao Wen^{1

2}

Affiliations

¹ State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
² Department of Hepatobiliary and Hydatid Disease, Digestive and Vascular Surgery Center Therapy Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.

Abstract

Ghrelin widely exists in the central nervous system and peripheral organs, and has biological activities such as maintaining energy homeostasis, regulating lipid metabolism, cell proliferation, immune response, gastrointestinal physiological activities, cognition, memory, circadian rhythm and reward effects. In many benign liver diseases, it may play a hepatoprotective role against steatosis, chronic inflammation, oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress and apoptosis, and improve liver cell autophagy and immune response to improve disease progression. However, the role of Ghrelin in liver Echinococcosis is currently unclear. This review systematically summarizes the molecular mechanisms by which Ghrelin regulates liver growth metabolism, immune-inflammation, fibrogenesis, proliferation and apoptosis, as well as its protective effects in liver fibrosis diseases, and further proposes the role of Ghrelin in liver Echinococcosis infection. During the infectious process, it may promote the parasitism and survival of parasites on the host by improving the immune-inflammatory microenvironment and fibrosis state, thereby accelerating disease progression. However, there is currently a lack of targeted in vitro and in vivo experimental evidence for this viewpoint.

Keywords: Echinococcosis; Ghrelin; IGF - I; fibrosis; liver.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Disease Progression
Echinococcosis*
Ghrelin*
Humans
Inflammation
Liver Cirrhosis

Substances

Ghrelin

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The work was funded by the National Natural Science Foundation of China (82160395), the China Postdoctoral Science Foundation (2022MD723847), the Xinjiang Uygur Autonomous Region Key R&D Programme Projects (2022B03013-4) and the Natural Science Foundation of Xinjiang Uygur Autonomous Region, China (2023D01A120).