International Journal of Molecular Sciences

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New Insights into Liver Biology and Disease Pathogenesis: Shedding Light on Novel Diagnostic and Therapeutic Approaches

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Dear Colleagues,

Despite advances in diagnosis, treatment, and prevention, diseases of the liver and biliary tract are still a significant cause of death worldwide. The recent 2023 Global Burden of Liver Diseases estimates that 4% of all deaths are attributed to liver diseases. Understanding basic liver molecular biology and disease pathogenesis can help us to identify novel biomarkers, improve diagnosis, and develop novel therapies and prevention strategies. In the past few years, single-cell transcriptomics, advanced culture systems, and CRISPR technology have enabled our community to start deciphering the molecular mechanisms underlying liver regeneration, repair, and carcinogenesis that could lead to clinical interventions to improve the quality of life of patients with liver diseases and reduce mortality.

This Special Issue aims to gather a collection of state-of-the-art and up-to-date articles covering recent advances in liver molecular biology and disease pathogenesis, including topics related to liver regeneration, repair, and carcinogenesis, the brain–gut–liver axis, novel therapeutic targets and interventions, diagnostic tools and morbidity biomarkers, host–pathogen interactions, and novel in vitro and in vivo models of liver diseases. Submission of basic and translational original research articles and reviews are welcome. Studies on liver diseases induced by infectious agents and on steatotic liver diseases are also encouraged.

Dr. Thiago Almeida Pereira
Guest Editor

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Research

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12 pages, 4455 KiB

Open AccessArticle

HMGB1-Mediated Cell Death—A Crucial Element in Post-Hepatectomy Liver Failure

by Laura Brunnthaler, Thomas G. Hammond, David Pereyra, Jonas Santol, Joel Probst, Valerie Laferl, Ulrike Resch, Monika Aiad, Anna Sofie Janoschek, Thomas Gruenberger, Hubert Hackl, Patrick Starlinger and Alice Assinger

Int. J. Mol. Sci. 2024, 25(13), 7150; https://doi.org/10.3390/ijms25137150 - 28 Jun 2024

Cited by 1 | Viewed by 1074

Abstract

Liver resection (LR) is the primary treatment for hepatic tumors, yet posthepatectomy liver failure (PHLF) remains a significant concern. While the precise etiology of PHLF remains elusive, dysregulated inflammatory processes are pivotal. Therefore, we explored the theragnostic potential of extracellular high-mobility-group-box protein 1 (HMGB1), a key damage-associated molecular pattern (DAMP) released by hepatocytes, in liver recovery post LR in patients and animal models. Plasma from 96 LR patients and liver tissues from a subset of 24 LR patients were analyzed for HMGB1 levels, and associations with PHLF and liver injury markers were assessed. In a murine LR model, the HMGB1 inhibitor glycyrrhizin, was administered to assess its impact on liver regeneration. Furthermore, plasma levels of keratin-18 (K18) and cleaved cytokeratin-18 (ccK18) were quantified to assess suitability as predictive biomarkers for PHLF. Patients experiencing PHLF exhibited elevated levels of intrahepatic and circulating HMGB1, correlating with markers of liver injury. In a murine LR model, inhibition of HMGB1 improved liver function, reduced steatosis, enhanced regeneration and decreased hepatic cell death. Elevated levels of hepatic cell death markers K18 and ccK18 were detected in patients with PHLF and correlations with levels of circulating HMGB1 was observed. Our study underscores the therapeutic and predictive potential of HMGB1 in PHLF mitigation. Elevated HMGB1, K18, and ccK18 levels correlate with patient outcomes, highlighting their predictive significance. Targeting HMGB1 enhances liver regeneration in murine LR models, emphasizing its role in potential intervention and prediction strategies for liver surgery. Full article

(This article belongs to the Special Issue New Insights into Liver Biology and Disease Pathogenesis: Shedding Light on Novel Diagnostic and Therapeutic Approaches)

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13 pages, 1147 KiB

Open AccessReview

Current Evidence and Perspectives of Cluster of Differentiation 44 in the Liver’s Physiology and Pathology

by Jinsol Han, Chanbin Lee and Youngmi Jung

Int. J. Mol. Sci. 2024, 25(9), 4749; https://doi.org/10.3390/ijms25094749 - 26 Apr 2024

Cited by 1 | Viewed by 1458

Abstract

Cluster of differentiation 44 (CD44), a multi-functional cell surface receptor, has several variants and is ubiquitously expressed in various cells and tissues. CD44 is well known for its function in cell adhesion and is also involved in diverse cellular responses, such as proliferation, migration, differentiation, and activation. To date, CD44 has been extensively studied in the field of cancer biology and has been proposed as a marker for cancer stem cells. Recently, growing evidence suggests that CD44 is also relevant in non-cancer diseases. In liver disease, it has been shown that CD44 expression is significantly elevated and associated with pathogenesis by impacting cellular responses, such as metabolism, proliferation, differentiation, and activation, in different cells. However, the mechanisms underlying CD44’s function in liver diseases other than liver cancer are still poorly understood. Hence, to help to expand our knowledge of the role of CD44 in liver disease and highlight the need for further research, this review provides evidence of CD44’s effects on liver physiology and its involvement in the pathogenesis of liver disease, excluding cancer. In addition, we discuss the potential role of CD44 as a key regulator of cell physiology. Full article

(This article belongs to the Special Issue New Insights into Liver Biology and Disease Pathogenesis: Shedding Light on Novel Diagnostic and Therapeutic Approaches)

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