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Molecular Advances in Liver Fibrosis
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Molecular Advances in Liver Fibrosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 2047

Special Issue Editor

Dr. Domenica Mangieri

E-Mail Website
Guest Editor
Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy
Interests: cancer biology and therapy; angiogenesis/anti-angiogenesis; chemoprevention
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Liver fibrosis (LF) is a multifactorial, fibro-inflammatory disorder characterized by exacerbated production of extracellular matrix with consequent aberration of hepatic tissue. The aetiology of this disease is very complex and seems to involve a broad spectrum of factors including the lifestyle, environment factors, genes and epigenetic changes. Recent evidences indicate that angiogenesis plays a crucial role in the progression of LF. Central to the pathogenesis of LF is the the activation of hepatic stellate cells (HSCs) which represent a crossroad among inflammation, fibrosis and angiogenesis. Quiescent HSCs can be stimulated by a host of growth factors, pro-inflammatory mediators produced by damaged resident liver cell types, as well as by hypoxia, contributing to neoangiogenesis, which in turn can be a bridge between acute and chronic inflammation. LF is currently treated with synthetic anti- fibrotic drugs related to inhibiting HSCs activation and proliferation; however LF may be prevented or reversed by several bioactive and natural compounds due to their antioxidant, anti-angiogenetic and anti-inflammatory features and, also, to their ability to revert the activated forms of HSCs in a more quiescent phenotype.

The intent of the Special Issue is to discuss the cause and the role of angiogenesis in LF focusing on the current knowledge about the impact of anti-angiogenetic therapies not neglecting the employ of natural compounds.

Dr. Domenica Mangieri
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • liver fibrosis
  • inflammation
  • hypoxia
  • angiogenesis
  • hepatic stellate cells
  • drug therapy
  • natural compounds
  • phytochemicals

Published Papers (2 papers)

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Research

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10 pages, 3664 KiB  
Communication
The Dual-Mode Transition of Myofibroblasts Derived from Hepatic Stellate Cells in Liver Fibrosis
by Mengchao Yan, Ye Xie, Jia Yao and Xun Li
Int. J. Mol. Sci. 2023, 24(20), 15460; https://doi.org/10.3390/ijms242015460 - 23 Oct 2023
Cited by 1 | Viewed by 891
Abstract
Hepatic stellate cells (HSCs) are the key promoters of liver fibrosis. In response to liver-fibrosis-inducing factors, HSCs express alpha smooth muscle actin (α-SMA) and obtain myofibroblast phenotype. Collagen secretion and high expression of α-SMA with related high cell tension and migration limitation are [...] Read more.
Hepatic stellate cells (HSCs) are the key promoters of liver fibrosis. In response to liver-fibrosis-inducing factors, HSCs express alpha smooth muscle actin (α-SMA) and obtain myofibroblast phenotype. Collagen secretion and high expression of α-SMA with related high cell tension and migration limitation are the main characteristics of myofibroblasts. How these two characteristics define the role of myofibroblasts in the initiation and progression of liver fibrosis is worth exploring. From this perspective, we explored the correlation between α-SMA expression and collagen secretion in myofibroblasts and the characteristics of collagen deposition in liver fibrosis. Based on a reasonable hypothesis and experimental verification, we believe that the myofibroblast with the α-SMAhighcollagenhigh model do not effectively explain the initial stage and progression characteristics of liver fibrosis. Therefore, we propose a myofibroblast dual-mode transition model in fibrotic liver (DMTM model). In the DMTM model, myofibroblasts have dual modes. Myofibroblasts obtain enhanced α-SMA expression, accompanied by collagen expression inhibition in the high-concentration region of TGF-β. At the edge of the TGF-β positive region, myofibroblasts convert to a high-migration and high-collagen secretion phenotype. This model reasonably explains collagen deposition and expansion in the initial stage of liver fibrosis. Full article
(This article belongs to the Special Issue Molecular Advances in Liver Fibrosis)
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Review

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15 pages, 1350 KiB  
Review
Redox Biology and Liver Fibrosis
by Francesco Bellanti, Domenica Mangieri and Gianluigi Vendemiale
Int. J. Mol. Sci. 2024, 25(1), 410; https://doi.org/10.3390/ijms25010410 - 28 Dec 2023
Cited by 1 | Viewed by 754
Abstract
Hepatic fibrosis is a complex process that develops in chronic liver diseases. Even though the initiation and progression of fibrosis rely on the underlying etiology, mutual mechanisms can be recognized and targeted for therapeutic purposes. Irrespective of the primary cause of liver disease, [...] Read more.
Hepatic fibrosis is a complex process that develops in chronic liver diseases. Even though the initiation and progression of fibrosis rely on the underlying etiology, mutual mechanisms can be recognized and targeted for therapeutic purposes. Irrespective of the primary cause of liver disease, persistent damage to parenchymal cells triggers the overproduction of reactive species, with the consequent disruption of redox balance. Reactive species are important mediators for the homeostasis of both hepatocytes and non-parenchymal liver cells. Indeed, other than acting as cytotoxic agents, reactive species are able to modulate specific signaling pathways that may be relevant to hepatic fibrogenesis. After a brief introduction to redox biology and the mechanisms of fibrogenesis, this review aims to summarize the current evidence of the involvement of redox-dependent pathways in liver fibrosis and focuses on possible therapeutic targets. Full article
(This article belongs to the Special Issue Molecular Advances in Liver Fibrosis)
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