Chronic hepatitis B virus (HBV) infection is a major risk factor for liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Despite advances in understanding HBV-related liver diseases, effective therapeutic strategies remain limited. Macrophage migration inhibitory factor (MIF) has been implicated in various inflammatory and fibrotic conditions, but its role in HBV-induced liver fibrosis has not been fully explored. This study investigates the involvement of MIF in liver fibrosis and evaluates its potential as a therapeutic target. We found that MIF expression was significantly elevated in hepatic stellate cells (HSCs) following stimulation with HBVcc (HBV cell culture) or HBV surface antigen (HBsAg). Through its receptor CD74, MIF enhanced the TGF-β/SMAD signaling pathway, promoting HSC activation and liver fibrosis progression. Histological analysis revealed higher MIF and CD74 expression in HBsAg-positive individuals compared to HBsAg-negative controls. Moreover, MIF expression correlated with the activation of fibrosis markers, including α-SMA and TGF-β-related proteins. Inhibition of MIF with the specific inhibitor ISO-1 attenuated fibrosis progression, suggesting that targeting MIF could offer a promising approach for treating HBV-related liver fibrosis. Our findings underscore the critical role of the MIF/CD74 axis in liver fibrosis and provide a basis for future therapeutic strategies targeting MIF in chronic liver diseases.

Current Issues in Molecular Biology

MIF Inhibition by ISO-1 Decreased Autophagic Activity in Primary Astrocytes During Cobalt Chloride-Induced Hypoxia

Article

Author: Cho, Hye-Ji ; Lee, Jung-Ho ; Park, Ji-Hyun ; Song, Dae-Yong ; Yoo, Hong-Il

Ischemic stroke is a leading contributor to death and disability worldwide, driving extensive research into pharmacological treatments beyond thrombolysis. Macrophage migration inhibitory factor (MIF), a cytokine, is implicated in several pathological conditions. In this study, we examined the effects of MIF on autophagy in astrocytes under the condition of chemical hypoxia. Primary astrocytes were treated with cobalt chloride, a well-known drug for inducing chemical hypoxia, followed by Western blot analyses to assess the HIF-1α, MIF, and LC3 protein levels along with a CCK assay. Additionally, cobalt chloride-treated astrocytes were co-treated with the MIF inhibitor ISO-1, and Western blot analyses were performed for MIF and LC3. Cell viability was evaluated using the CCK assay in astrocytes treated with cobalt chloride and ISO-1, with additional rapamycin treatment. Our results show that ISO-1 reduced LC3-II levels in astrocytes exposed to high concentrations of cobalt chloride (1000 μM) for 6 h. Moreover, rapamycin decreased cell viability in astrocytes treated with both 1000 μM cobalt chloride and ISO-1. Our data suggest that MIF plays a role in inducing autophagy in astrocytes under hypoxic conditions and is involved in the regulation of autophagic activity.

Journal of Materials Chemistry B

Dual-modality probe nanodrug delivery systems with ROS-sensitivity for atherosclerosis diagnosis and therapy.

Article

Author: Li, Yapeng ; Wang, Jingyuan ; Zhao, Yan ; Liu, Linlin ; Jiang, Hui ; Shen, Meili ; Yang, Haiqin ; Meng, Hao ; Yang, Qingbiao ; Li, Shaojing

Most acute cardiovascular and cerebrovascular diseases are caused by atherosclerotic plaque rupture leading to blocked arteries. Targeted nanodelivery systems deliver imaging agents or drugs to target sites for diagnostic imaging or the treatment of various diseases, providing new insights for the detection and treatment of atherosclerosis. Based on the pathological characteristics of atherosclerosis, a hydrogen peroxide-sensitive bimodal probe PPIS@FC with integrated diagnosis and treatment function was designed. Bimodal probes Fe₃O₄@SiO₂-CDs (FC) were prepared by coupling superparamagnetic iron oxide and carbon quantum dots synthesized with citric acid, and self-assembled with hydrogen peroxide stimulus-responsive amphiphilic block polymer PGMA-PEG modified with simvastatin (Sim) and target molecule ISO-1 to obtain drug-loaded micelles PGMA-PEG-ISO-1-Sim@FC (PPIS@FC). PPIS@FC could release Sim and FC in an H₂O₂-triggered manner, achieving the goal of releasing drugs using the special microenvironment at the plaque. At the same time, in vivo magnetic resonance and fluorescence imaging results proved that PPIS@FC possessed targeting ability, magnetic resonance imaging and fluorescence imaging effects. The results of the FeCl₃ and ApoE^-/- model showed that PPIS@FC had an excellent therapeutic effect and in vivo safety. Therefore, dual-modality imaging drug delivery systems with ROS response will become a promising strategy for the diagnosis and treatment of atherosclerosis.

100 Deals associated with ISO-1

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Indication	Highest Phase	Country/Location	Organization	Date
Prostatitis	Preclinical	CN	Anhui Medical University	01 Nov 2024
Intervertebral Disc Degeneration	Preclinical	CN	Jiangsu University	01 Jun 2024
Intervertebral Disc Degeneration	Preclinical	CN	Soochow University	01 Jun 2024
Myositis	Preclinical	AU	Griffith University	05 Jul 2011
Myositis	Preclinical	AU	University of Canberra	05 Jul 2011
Ross River Fever	Preclinical	AU	Griffith University	05 Jul 2011
Ross River Fever	Preclinical	AU	University of Canberra	05 Jul 2011

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