Qu RH, Rong Y, Ni WZ, Huang XL, Chen YZ, Li HF. Fibrinogen superfamily proteins: Key regulators in hepatic disorders. World J Exp Med 2025; 15(3): 106677 [DOI: 10.5493/wjem.v15.i3.106677]
Corresponding Author of This Article
Hai-Fang Li, Associate Professor, College of Life Sciences, Shandong Agricultural University, No. 61 Daizong Street, Tai’an 271018, Shandong Province, China. haifangli@sdau.edu.cn
Research Domain of This Article
Biology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Exp Med. Sep 20, 2025; 15(3): 106677 Published online Sep 20, 2025. doi: 10.5493/wjem.v15.i3.106677
Fibrinogen superfamily proteins: Key regulators in hepatic disorders
Rong-Hui Qu, Yi Rong, Wen-Zhe Ni, Xing-Lin Huang, Yi-Zhuo Chen, Hai-Fang Li
Rong-Hui Qu, Yi Rong, Wen-Zhe Ni, Xing-Lin Huang, Yi-Zhuo Chen, Hai-Fang Li, College of Life Sciences, Shandong Agricultural University, Tai’an 271018, Shandong Province, China
Co-first authors: Rong-Hui Qu and Yi Rong.
Author contributions: Qu RH and Rong Y revised the manuscript, and they contributed equally to this article as co-first authors; Qu RH, Rong Y, Ni WZ, Huang XL, and Chen YZ wrote the original draft; Li HF supervised, conceived, verified, reviewed, and edited the manuscript; All authors were involved in the critical review of the results and have read and approved the final manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hai-Fang Li, Associate Professor, College of Life Sciences, Shandong Agricultural University, No. 61 Daizong Street, Tai’an 271018, Shandong Province, China. haifangli@sdau.edu.cn
Received: March 4, 2025 Revised: April 18, 2025 Accepted: June 20, 2025 Published online: September 20, 2025 Processing time: 161 Days and 6.3 Hours
Abstract
Liver diseases including hepatic injury, hepatitis, metabolic-associated fatty liver disease, and hepatocellular carcinoma have emerged as critical public health challenges globally. The fibrinogen (FG) superfamily proteins, primarily comprising FG, FG-like protein (FGL) 1, and FGL2, have been demonstrated to exert regulatory effects on hepatic tissue regeneration, lipid metabolism homeostasis, and oncogenic processes in hepatocytes. This review systematically examines the pathophysiological correlations between FG superfamily members and major hepatic disorders. Physiologically, FG superfamily proteins function as hepatoprotective mediators through their intrinsic capacity to enhance hepatic parenchymal regeneration and extracellular matrix remodeling. However, emerging evidence reveals their dual regulatory properties, whereby overactivation of these hepatokines paradoxically induces a pathological shift characterized by pro-inflammatory cascades, metabolic derangement potentiation, and tumor invasion and metastasis promotion. Specifically, we elucidate the molecular mechanisms underlying their involvement in hepatitis progression, metabolic-associated fatty liver disease pathogenesis, and hepatocellular carcinoma tumorigenesis. Furthermore, we highlight their therapeutic potential in hepatic disease management, particularly emphasizing that targeting the FGL1/lymphocyte activation gene 3 immune checkpoint axis represents a novel paradigm in precision cancer immunotherapy.
Core Tip: In this article, we introduce three fibrinogen superfamily proteins: Fibrinogen, FG-like protein 1, and FG-like protein 2. We focus on their roles in liver injury, metabolic associated fatty liver disease, and hepatocellular carcinoma, as well as potential therapeutic approaches. This review aims to deepen the understanding of the relationship between the fibrinogen superfamily and liver diseases, providing new insights for the treatment of hepatic disorders.
