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    Mini-Review Open Access
    Efficacy of Addiction Pharmacotherapy in Alcohol Use Disorder and Their Effects on Liver Health
    Jiahua Zhou, Jiajing Li, Qiuwei Pan, Ibrahim Ayada
    Journal of Clinical and Translational Hepatology, Published online July 1, 2024. doi:10.14218/JCTH.2024.00059
    Abstract
    Both alcohol-associated liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease are leading contributors to chronic liver diseases. These conditions often [...] Read more.

    Both alcohol-associated liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease are leading contributors to chronic liver diseases. These conditions often coexist, exacerbating disease progression. Despite ALD being a leading cause of liver transplantation, many individuals with alcohol use disorder (AUD) do not receive treatment. In this review, we discussed the epidemiology of ALD in AUD, various treatment options for AUD, and their efficacy on liver health. Our critical analysis of current evidence underscores the need for integrated models involving multiple stakeholders to improve ALD management.

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    Review Article Open Access
    Inter-variant Recombination, Genomic Perspectives and Pathogenicity of Emerging Sub-variants of Omicron: Recent Updates and Challenges
    Gourab Das, Rubai Ahmed, Jhimli Banerjee, Sovan Samanta, Swarnali Das, Saheli Pramanik, Balaram Das, Biplab Giri, Sandeep Kumar Dash
    Gene Expression, Published online June 30, 2024. doi:10.14218/GE.2023.00104
    Abstract
    The years 2019–2021 of the twenty-first century are synonymous with the COVID era, as the Coronavirus disease 2019 (COVID-19) wreaked havoc and continues to be aggressively persecuted. [...] Read more.

    The years 2019–2021 of the twenty-first century are synonymous with the COVID era, as the Coronavirus disease 2019 (COVID-19) wreaked havoc and continues to be aggressively persecuted. Globally, about 300 million COVID-19 cases and nearly 5.3 million fatalities have been recorded so far. Since then, the coronavirus RNA genome has rapidly mutated, giving rise to several mutant and recombinant variants. On March 9, 2022, a new recombinant known as Deltacron/Delmicron emerged due to inter-lineage recombination between Delta and Omicron. Many researchers consider it a “grey rhino” occurrence rather than a “black swan” event. However, some groups of scientists claim it is a “laboratory error”. Another COVID-19 variant, XE (a recombination of BA.1 and BA.2), has been discovered, which has a transmission rate ten times higher than the fastest-spreading Omicron subvariant BA.2. Delta and Omicron, two of the most novel strains, co-circulated for many weeks in several parts of the globe, allowing for coinfections and eventual recombination. Consequently, the recombinant strains XD and XF are associated with a very high transmission rate and reduced neutralizing antibody response. Under these circumstances, researchers are rushing to develop a vaccine with high efficacy against the circulating mutants and the variants likely to emerge in the near future. This review article provides recent updates on newly identified sub-variants of Omicron with an in-depth focus on their genomic alterations, infectivity patterns, and pathogenic manifestations.

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    Review Article Open Access
    Molecular Targets of microRNAs during Liver Regeneration after Acute Injury: Recent Advances
    Roberto Loi, Gabriella Simbula, Monica Pibiri
    Gene Expression, Published online June 30, 2024. doi:10.14218/GE.23.00175
    Abstract
    Experimental models using 2/3 partial hepatectomy or chemical injury have helped identify the pathways associated with liver regeneration (LR). Several microRNAs (miRNAs) have been [...] Read more.

    Experimental models using 2/3 partial hepatectomy or chemical injury have helped identify the pathways associated with liver regeneration (LR). Several microRNAs (miRNAs) have been identified as modulators of LR, but the molecular mechanisms underlying their activity are still unclear. Given the development of new therapies targeting miRNAs, this is an important question to address. This review discusses recent studies exploring the molecular mechanisms of miRNA-dependent regulation of LR. In particular, the finding that circ-RBM23 promotes LR by sequestering cytoplasmic miRNA139-5p has furthered the understanding of the molecular mechanisms underlying circRNA activity. Interestingly, although miRNAs are generally considered negative regulators of their target mRNAs, miRNAs182-5p promotes LR by upregulating Cyp7a. Furthermore, mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) were shown to enhance LR after 2/3 partial hepatectomy by releasing miRNAs that inhibit gene expression to promote an anti-inflammatory response or miRNA-regulatory factors. Since the administration of MSCs-EVs has no hepatotoxic side effects, this may represent a therapeutic strategy to promote LR. miRNAs also mediate LR after chemical injury. This is the case for miR194 and miR21, whose downregulation activates pro-regeneration pathways to ameliorate acetaminophen-induced liver injury. In addition, the downregulation of miR21 has been shown to improve autophagy and haemostasis after acetaminophen overdose. Although further studies are needed to improve their efficacy as therapeutics, the evidence gathered in this review has led to a better understanding of the molecular mechanisms associated with the control of LR by miRNAs.

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    Review Article Open Access
    Environmental Triggers’ Involvement in the Development of Type 1 Diabetes Mellitus
    Tajudeen Olanrewaju Yahaya, Umar Usman Liman, Caleb Dikko Obadiah, Zafira Illo Zakari, Daniel Anyebe, Boniface Gomo Clement, Balkisu Marafa Muhammad
    Exploratory Research and Hypothesis in Medicine, Published online July 27, 2022. doi:10.14218/ERHM.2022.00051
    Abstract
    The huge burden of type 1 diabetes mellitus (T1DM) has been a source of concern globally since the Industrial Revolution in the 18th–19th centuries. To this end, studies have shown [...] Read more.

    The huge burden of type 1 diabetes mellitus (T1DM) has been a source of concern globally since the Industrial Revolution in the 18th–19th centuries. To this end, studies have shown that certain environmental changes that accompanied the Revolution may have increased the risk and burden of the disease in genetically predisposed individuals. However, documented studies that synthesize these environmental triggers are scarce. As a result, the current study was conceived to synthesize the environmental triggers of T1DM to boost public awareness. Relevant information was retrieved from reputable academic databases; namely, Scopus, PubMed, SpringerLink, and Embase. The results showed that chemical exposure, viral infection, gut microbiome disruption, vitamin and mineral deficiencies, inadequate or exclusive breastfeeding, as well as early exposure to infant feeding formulas could increase the risk and burden of T1DM in genetically predisposed individuals. As a consequence, these triggers could compromise the expression of certain genes involved in insulin synthesis and immune function, such as the human leukocyte antigen (HLA), insulin (INS), cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), and protein tyrosine phosphatase non-receptor type 22 (PTPN22) genes. This would result in a dysfunctional immune system in which immune cells, such as T-cells and B-cells and molecules, such as cytokines would attack self-tissues, thus causing autoimmunity of the pancreatic beta cells. Environmental triggers could also induce the T1DM pathophysiology by modifying the epigenome of the mentioned genes. Furthermore, some epigenetic changes could be reversed, which would infer that treatment procedures that would include the pathophysiology of the environmental triggers could be more effective.

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    Original Article Open Access
    Overexpression of RBM34 Promotes Tumor Progression and Correlates with Poor Prognosis of Hepatocellular Carcinoma
    Wei Wang, Rui Zhang, Ning Feng, Longzhen Zhang, Nianli Liu
    Journal of Clinical and Translational Hepatology, Published online July 13, 2022. doi:10.14218/JCTH.2022.00166
    Abstract
    Emerging evidence suggests that RNA-binding motif (RBM) proteins are involved in hepatocarcinogenesis and act either as oncogenes or tumor suppressors. The objective of this study [...] Read more.

    Emerging evidence suggests that RNA-binding motif (RBM) proteins are involved in hepatocarcinogenesis and act either as oncogenes or tumor suppressors. The objective of this study was to investigate the role of RBM34, an RBM protein, in hepatocellular carcinoma (HCC).

    We first examined the expression of RBM34 across cancers. The correlation of RBM34 with clinicopathological features and the prognostic value of RBM34 for HCC was then investigated. Functional enrichment analysis of RBM34-related differentially expressed genes (DEGs) was performed to explore its biological function. RNA sequencing (RNA-seq) was applied to identify downstream genes and pathways affected upon RBM34 knockout. The correlation of RBM34 with immune characteristics was also analyzed. The oncogenic function of RBM34 was examined in in vitro and in vivo experiments.

    RBM34 was highly expressed in hepatocellular carcinoma and correlated with poor clinicopathological features and prognosis. RBM34 was positively associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression. A positive correlation was also observed between RBM34, T cell exhaustion, and regulatory T cell marker genes. Knockout of RBM34 significantly inhibited cell proliferation, migration, and xenograft tumor growth, and sensitized HCC cells to sorafenib treatment. RBM34 inhibition reduced FGFR2 expression and affected PI3K-AKT pathway activation in HCC cells.

    Our study suggests that RBM34 may serve as a new prognostic marker and therapeutic target of HCC.

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    Original Article Open Access
    Naringenin is a Potential Immunomodulator for Inhibiting Liver Fibrosis by Inhibiting the cGAS-STING Pathway
    Li Chen, Siwei Xia, Shuqi Wang, Yuanyuan Zhou, Feixia Wang, Zhanghao Li, Yang Li, Desong Kong, Zili Zhang, Jiangjuan Shao, Xuefen Xu, Feng Zhang, Shizhong Zheng
    Journal of Clinical and Translational Hepatology, Published online April 28, 2022. doi:10.14218/JCTH.2022.00120
    Abstract
    Naringenin is an anti-inflammatory flavonoid that has been studied in chronic liver disease. The mechanism specific to its antifibrosis activity needs further investigation This [...] Read more.

    Naringenin is an anti-inflammatory flavonoid that has been studied in chronic liver disease. The mechanism specific to its antifibrosis activity needs further investigation This study was to focused on the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) pathway in hepatic stellate cells and clarified the antifibrosis mechanism of naringenin.

    The relationship between the cGAS-stimulator of interferon genes (STING) pathway and liver fibrosis was analyzed using the Gene Expression Omnibus database. Histopathology, immunohistochemistry, fluorescence staining, Western blotting and polymerase chain reaction were performed to assess gene and protein expression levels associated with the cGAS pathway in clinical liver tissue samples and mouse livers. Molecular docking was performed to evaluate the relationship between naringenin and cGAS, and western blotting was performed to study the expression of inflammatory factors downstream of cGAS in vitro.

    Clinical database analyses showed that the cGAS-STING pathway is involved in the occurrence of chronic liver disease. Naringenin ameliorated liver injury and liver fibrosis, decreased collagen deposition and cGAS expression, and inhibited inflammation in carbon tetrachloride (CCl4)-treated mice. Molecular docking found that cGAS may be a direct target of naringenin. Consistent with the in vivo results, we verified the inhibitory effect of naringenin on activated hepatic stellate cells (HSCs). By using the cGAS-specific agonist double-stranded (ds)DNA, we showed that naringenin attenuated the activation of cGAS and its inflammatory factors affected by dsDNA. We verified that naringenin inhibited the cGAS-STING pathway, thereby reducing the secretion of inflammatory factors by HSCs to ameliorate liver fibrosis.

    Interrupting the cGAS-STING pathway helped reverse the fibrosis process. Naringenin has potential as an antihepatic fibrosis drug.

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Special Features

Call for Papers for Special Issue 'Updates of Cytopathology Reporting Systems'

Journal: Journal of Clinical and Translational Pathology
Special Issue: Updates of Cytopathology Reporting Systems
Submission deadline: November 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Frontier research on the toxicity and efficacy of Chinese medicine'

Journal: Future Integrative Medicine
Special Issue: Frontier research on the toxicity and efficacy of Chinese medicine
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘New Translational Challenges in Primary Biliary Cholangitis’

Journal: Journal Clinical and Translational Hepatology
Special Issue: New Translational Challenges in Primary Biliary Cholangitis
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘A Spotlight on Progress and Pitfalls in NAFLD/MAFLD Studies, 2022’

Journal: Journal of Clinical and Translational Hepatology
Special Issue: A Spotlight on Progress and Pitfalls in NAFLD/MAFLD Studies, 2022
Submission deadline: March 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Comparative study of traditional medicine in the world'

Journal: Future Integrative Medicine
Special Issue: Comparative study of traditional medicine in the world
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Therapeutic effects of herbal medicines on neurological impairment and related mental disorders based on the evidence of clinical and basic studies'

Journal: Future Integrative Medicine
Special Issue: Therapeutic effects of herbal medicines on neurological impairment and related mental disorders based on the evidence of clinical and basic studies
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘Immunoregulatory Mechanisms of Herbal Medicines in Cancer and Infectious Diseases’

Journal: Future Integrative Medicine
Special Issue: Immunoregulatory Mechanisms of Herbal Medicines in Cancer and Infectious Diseases
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted
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