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Original Article Open Access
Qiangqiang Zhao, Feihong Che, Hongxiao Li, Rihe Hu, Liuchao Hu, Qiushi Wei, Liangliang Xu, Yamei Liu
Published online March 25, 2025
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Future Integrative Medicine. doi:10.14218/FIM.2024.00049
Abstract
Huo Xue Tong Luo Capsule (HXTL) has been clinically used to treat osteonecrosis of the femoral head, osteoporosis, and other bone and joint diseases with promising effects. Our [...] Read more.

Huo Xue Tong Luo Capsule (HXTL) has been clinically used to treat osteonecrosis of the femoral head, osteoporosis, and other bone and joint diseases with promising effects. Our previous study has shown that HXTL can promote osteogenesis in mesenchymal stem cells by inhibiting lncRNA-Miat expression through histone modifications. However, the mechanism by which HXTL treats postmenopausal osteoporosis (PMOP) remains unclear. In this study, we used network pharmacology-based mechanism prediction, molecular docking, and pharmacological validation to investigate the mechanism of HXTL in treating PMOP.

The key candidate targets and relevant signaling pathways of HXTL for PMOP treatment were predicted using network pharmacology and molecular docking analysis. RAW264.7 cells were used for Western blot to validate the predicted mechanistic pathways. The ovaries of mice were surgically removed to simulate PMOP. The effect of HXTL on PMOP was evaluated using tartrate-resistant acid phosphatase staining and immunohistochemical assays in vivo.

Network pharmacology analysis suggested that HXTL interacted with 215 key targets linked to PMOP, primarily affecting the PI3K-AKT signaling pathway. Molecular docking showed that the main components of HXTL exhibited strong binding affinity to NFATc1, p-PI3K, and p-AKT1. Furthermore, our in vitro results confirmed that HXTL suppressed the PI3K-AKT signaling pathway. In vivo, HE and tartrate-resistant acid phosphatase staining results showed that HXTL inhibited osteoclast formation and protected bone mass.

This research demonstrated that HXTL could inhibit osteoclast formation and prevent bone loss induced by ovariectomy in mice by inhibiting the PI3K-AKT signaling pathway. These findings provide important evidence for the clinical application of HXTL in treating PMOP.

Full article
Original Article Open Access
Rong Fan, Ya-Ru Shi, Lei Chen, Chuan-Xin Wang, Yun-Song Qian, Yan-Hang Gao, Chun-Ying Wang, Xiao-Tang Fan, Xiao-Long Liu, Hong-Lian Bai, Dan Zheng, Guo-Qing Jiang, Yan-Long Yu, Xie-Er Liang, Jin-Jun Chen, Wei-Fen Xie, Lu-Tao Du, Hua-Dong Yan, Yu-Jin Gao, Hao Wen, Jing-Feng Liu, Min-Feng Liang, Fei Kong, Jian Sun, Sheng-Hong Ju, Hong-Yang Wang, Jin-Lin Hou
Published online August 1, 2025
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00091
Abstract
Given the high burden of hepatocellular carcinoma (HCC), risk stratification in patients with cirrhosis is critical but remains inadequate. In this study, we aimed to develop and [...] Read more.

Given the high burden of hepatocellular carcinoma (HCC), risk stratification in patients with cirrhosis is critical but remains inadequate. In this study, we aimed to develop and validate an HCC prediction model by integrating radiomics and deep learning features from liver and spleen computed tomography (CT) images into the established age-male-ALBI-platelet (aMAP) clinical model.

Patients were enrolled between 2018 and 2023 from a Chinese multicenter, prospective, observational cirrhosis cohort, all of whom underwent 3-phase contrast-enhanced abdominal CT scans at enrollment. The aMAP clinical score was calculated, and radiomic (PyRadiomics) and deep learning (ResNet-18) features were extracted from liver and spleen regions of interest. Feature selection was performed using the least absolute shrinkage and selection operator.

Among 2,411 patients (median follow-up: 42.7 months [IQR: 32.9–54.1]), 118 developed HCC (three-year cumulative incidence: 3.59%). Chronic hepatitis B virus infection was the main etiology, accounting for 91.5% of cases. The aMAP-CT model, which incorporates CT signatures, significantly outperformed existing models (area under the receiver-operating characteristic curve: 0.809–0.869 in three cohorts). It stratified patients into high-risk (three-year HCC incidence: 26.3%) and low-risk (1.7%) groups. Stepwise application (aMAP → aMAP-CT) further refined stratification (three-year incidences: 1.8% [93.0% of the cohort] vs. 27.2% [7.0%]).

The aMAP-CT model improves HCC risk prediction by integrating CT-based liver and spleen signatures, enabling precise identification of high-risk cirrhosis patients. This approach personalizes surveillance strategies, potentially facilitating earlier detection and improved outcomes.

Full article
Original Article Open Access
Simiao Yu, Sici Wang, Ping Li, Haocheng Zheng, Jing Jing, Tingting He, Xia Ding, Ruilin Wang
Published online June 30, 2025
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00073
Abstract
Drug-induced liver injury (DILI) represents a prevalent adverse event associated with medication use. However, the exact mechanisms underlying DILI remain incompletely understood, [...] Read more.

Drug-induced liver injury (DILI) represents a prevalent adverse event associated with medication use. However, the exact mechanisms underlying DILI remain incompletely understood, and the lack of specific diagnostic and prognostic biomarkers poses significant challenges to the clinical diagnosis and treatment of this condition. Consequently, our study aimed to endeavor to identify serum and fecal metabolic biomarkers, enabling more accurate DILI diagnosis and improved prediction of chronic progression.

Untargeted metabolomics analysis was performed on serum and fecal samples obtained from a cohort of 32 DILI patients (causality confirmed via the updated Roussel Uclaf Causality Assessment Method) and 36 healthy controls. Utilizing techniques such as partial least squares-discriminant analysis modeling and t-tests, we identified significantly differentially expressed metabolites and metabolite sets. Causality assessment was performed using the updated Roussel Uclaf Causality Assessment Method.

The findings from the analysis of serum and fecal metabolomics association pathways suggested that perturbations in bile acid metabolism might serve as potential mechanisms underlying the progression of DILI. Our study revealed 22 overlapping differential metabolites between serum and feces, displaying significant concentration differences between the DILI and healthy control groups. Notably, we identified chenodeoxycholic acid and deoxycholic acid as promising markers that not only distinguished DILI patients from healthy individuals but also exhibited predictive potential for DILI chronicity.

The integrated analysis of serum and fecal metabolites uncovers the significant disruption of bile acid metabolites as a key contributing factor in the pathogenesis of DILI. Our study offers promising potential biomarkers for the diagnosis and prognosis of DILI, paving the way for a novel perspective in the realm of DILI diagnosis and treatment.

Full article
Letter to the Editor Open Access
Ivan Rankovic, Vladimir Milivojevic, Jelena Martinov Nestorov, Nikola Panic, Jovanka Trifunovic, Christer Bäck, Elena Curakova Ristovska, Stefan Stojkovic, Salma Mudawi, Keith Siau
Published online December 15, 2024
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Journal of Translational Gastroenterology. doi:10.14218/JTG.2024.00013
Editorial Open Access
Amancio Carnero, Hua Wang
Published online January 15, 2025
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Gene Expression. doi:10.14218/GE.2025.00000
Original Article Open Access
Yani Wu, Yingnan Yang, Youju Zhang, Qiuran Xu, Dongsheng Huang, Kangsheng Tu
Published online February 11, 2025
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Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2024.00386
Abstract
General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating [...] Read more.

General transcription factor IIIC subunit 2 (GTF3C2) is one of the polymerase III transcription-related factors. Previous studies have revealed that GTF3C2 is involved in regulating cell proliferation. However, the role of GTF3C2 in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine its expression, biological function, and mechanism in HCC.

The expression of GTF3C2 in HCC and non-tumor tissues, along with its clinical significance, was investigated using public databases and clinical samples. Reverse transcription-quantitative polymerase chain reaction and Western blot assays were performed to detect the expression of GTF3C2, ubiquitin specific peptidase 21 (USP21), mitogen-activated protein kinase 2 (MEK2), extracellular signal-regulated kinase 1/2 (ERK1/2), and p-ERK1/2 in cells. A luciferase reporter assay was conducted to explore the regulatory effect of GTF3C2 on USP21 transcription. Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine, and colony formation assays were performed to assess HCC cell proliferation. Subcutaneous injection of HCC cells into nude mice was used to evaluate tumor growth in vivo.

GTF3C2 expression was upregulated in HCC tissues and was positively correlated with advanced tumor stages and high tumor grades. HCC patients with high GTF3C2 expression had significantly worse survival outcomes. Knockdown of GTF3C2 suppressed the proliferation of Hep3B and HCCLM3 cells, while overexpression of GTF3C2 facilitated the proliferation of SNU449 and Huh7 cells. GTF3C2 promoted USP21 expression by activating its transcription, which subsequently increased the levels of MEK2 and p-ERK1/2 in HCC cells. Overexpression of both USP21 and MEK2 counteracted the GTF3C2 knockdown-induced inactivation of the ERK1/2 pathway. Moreover, GTF3C2 promoted HCC cell proliferation in vitro and tumor growth in vivo by regulating the USP21/MEK2/ERK1/2 pathway.

Upregulation of GTF3C2 is frequently observed in HCC tissues and predicts poor prognosis. GTF3C2 promotes HCC cell proliferation via the USP21/MEK2/ERK1/2 pathway.

Full article
Editorial Open Access
Ben J. Gu
Published online March 25, 2025
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Journal of Exploratory Research in Pharmacology. doi:10.14218/JERP.2025.00000
Opinion Open Access
Tianhang Li, Xiaorui Chen, Ming Chen
Published online February 24, 2025
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Exploratory Research and Hypothesis in Medicine. doi:10.14218/ERHM.2024.00028
Original Article Open Access
Shuang Wu, Changmi Deng, Yufeng Han, Wen Fu, Ruixi Hua
Published online December 24, 2024
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Cancer Screening and Prevention. doi:10.14218/CSP.2024.00024
Abstract
Wilms tumor is the most common kidney tumor in children aged 0-14 years. MicroRNAs are small, noncoding RNAs linked to the development of malignant tumors. Several studies have [...] Read more.

Wilms tumor is the most common kidney tumor in children aged 0-14 years. MicroRNAs are small, noncoding RNAs linked to the development of malignant tumors. Several studies have shown the association between single nucleotide polymorphism in miR-27a and cancer risk. This study aimed to explore the potential impact of the miR-27a rs895819 T>C polymorphism on Wilms tumor susceptibility.

The rs895819 T>C polymorphism was genotyped using the TaqMan method in 145 patients with Wilms tumors and 531 controls. Logistic regression models were used to assess the association between this polymorphism and Wilms tumor risk. A stratified analysis was also performed based on age, sex, and clinical stage.

The rs895819 T>C polymorphism showed genotypic distribution consistent with Hardy-Weinberg equilibrium (P = 0.749). The differences were not statistically significant. The miR-27a rs895819 T>C polymorphism was not significantly associated with Wilms tumor susceptibility, and the stratified analysis did not yield any significant differences.

Our study provides evidence of a lack of association between the miR-27a rs895819 T>C polymorphism and Wilms tumor susceptibility. Further validation through larger sample sizes and additional genetic polymorphisms is warranted.

Full article
Letter to the Editor Open Access
Wenqing Yang
Published online December 18, 2024
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Journal of Exploratory Research in Pharmacology. doi:10.14218/JERP.2024.00023
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