Current Treatment Regimens and Promising Molecular Therapies for Chronic Hepatobiliary Diseases

Biomolecules, Год журнала: 2025, Номер 15(1), С. 121 - 121

Опубликована: Янв. 14, 2025

Chronic hepatobiliary damage progressively leads to fibrosis, which may evolve into cirrhosis and/or hepatocellular carcinoma. The fight against the increasing incidence of liver-related morbidity and mortality is challenged by a lack clinically validated early-stage biomarkers limited availability effective anti-fibrotic therapies. Current research focused on uncovering pathogenetic mechanisms that drive liver fibrosis. Drugs targeting molecular pathways involved in chronic diseases, such as inflammation, hepatic stellate cell activation proliferation, extracellular matrix production, are being developed. Etiology-specific treatments, those for hepatitis B C viruses, already clinical use, efforts develop new, targeted therapies other diseases ongoing. In this review, we highlight major changes occurring patients affected metabolic dysfunction-associated steatotic disease, viral (Delta virus), autoimmune (autoimmune hepatitis, primary biliary cholangitis, sclerosing cholangitis). Further, describe how knowledge linked current well ongoing preclinical novel strategies, including nucleic acid-, mesenchymal stromal/stem cell-, vesicle-based options. Much development obviously still missing, but plethora promising potential treatment strategies holds promise future reversal increase group patients.

Язык: Английский

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Expansion of Splice-Switching Therapy with Antisense Oligonucleotides

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(5), С. 2270 - 2270

Опубликована: Март 4, 2025

Since 2016, splice-switching therapy, in which splicing is controlled by antisense oligonucleotides, has been applied clinical practice for spinal muscular atrophy and Duchenne dystrophy. In the former disease, this therapy induces exon inclusion, while, latter, it skipping, leading expression of functional proteins. Basic studies many monogenic diseases have now conducted. The molecular mechanisms include not only induction inclusion but also pseudoexon skipping suppression sites generated mutations. addition, therapies that alter protein function regulating are being investigated non-monogenic ones such as cancer immune-related disorders. It expected these basic will be translated into applications. This review describes current status research applications to promote development treatments noncurable diseases.

Язык: Английский

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Engineered Intelligent Microenvironment Responsive Prodrug Conjugates Navigated by Bioinspired Lipoproteins for Reversing Liver Fibrosis

Small Methods, Год журнала: 2025, Номер unknown

Опубликована: Март 19, 2025

Abstract Liver fibrosis (LF) is characterized by excessive production of reactive oxygen species (ROS), abnormal activation hepatic stellate cells (HSCs), and subsequent extracellular matrix (ECM) deposition. The complexity multiple interrelated pathways involved in this process makes it challenging for monotherapy to achieve the desired therapeutic effects. To address issue, study designs a ROS‐activated heterodimer conjugate (VTO) collaboratively alleviate LF. Additionally, biomimetic high‐density lipoprotein utilized encapsulation, resulting formation PL‐VTO, which enables natural liver targeting. Once PL‐VTO delivered fibrotic liver, can respond release both parent drugs upon encountering high ROS microenvironment, effectively scavenge ROS, induce quiescence activated HSCs, reduce collagen deposition, ultimately reversing Overall, presents feasible versatile nanotherapeutic approach enhance prodrug‐driven treatment

Язык: Английский

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SRSF7 promotes pulmonary fibrosis through regulating PKM alternative splicing in lung fibroblasts

Acta Pharmaceutica Sinica B, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский

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Alternative splicing: hallmark and therapeutic opportunity in metabolic liver disease

Gastroenterology report, Год журнала: 2025, Номер 13

Опубликована: Янв. 1, 2025

Abstract Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the leading cause of chronic worldwide, with fibrosis recognized as main prognostic factor and therapeutic target. While early-stage is reversible, advanced poses a significant clinical challenge due to limited treatment options, highlighting need for innovative management strategies. Recent studies have shown that alternative pre-mRNA splicing, critical mechanism regulating gene expression protein diversity, plays fundamental role in pathogenesis MAFLD associated fibrosis. Understanding complex relationship between splicing progression could pave way novel approaches improve outcomes. In this review, we describe intricate mechanisms MAFLD. Specifically, explored pivotal factors, RNA-binding proteins, their interactions metabolic epigenetic regulators. Furthermore, provide an overview latest advancements splicing-based strategies biomarker development. Particular emphasis placed on potential application antisense oligonucleotides rectifying anomalies, thereby laying foundation precision medicine MAFLD-associated

Язык: Английский

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Shugan Jianpi Formula attenuate liver fibrosis via regulation of miR-193a-3p/TGF-β2 in hepatic stellate cells: An in vivo and in vitro study

Journal of Ethnopharmacology, Год журнала: 2024, Номер unknown, С. 119120 - 119120

Опубликована: Ноя. 1, 2024

Язык: Английский

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