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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: 20 May 2025 | Viewed by 10609

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

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Keywords

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

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Published Papers (4 papers)

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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 3 | Viewed by 1718
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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33 pages, 2382 KiB  
Review
Liver Fibrosis: From Basic Science towards Clinical Progress, Focusing on the Central Role of Hepatic Stellate Cells
by Hikmet Akkız, Robert K. Gieseler and Ali Canbay
Int. J. Mol. Sci. 2024, 25(14), 7873; https://doi.org/10.3390/ijms25147873 - 18 Jul 2024
Cited by 12 | Viewed by 4526
Abstract
The burden of chronic liver disease is globally increasing at an alarming rate. Chronic liver injury leads to liver inflammation and fibrosis (LF) as critical determinants of long-term outcomes such as cirrhosis, liver cancer, and mortality. LF is a wound-healing process characterized by [...] Read more.
The burden of chronic liver disease is globally increasing at an alarming rate. Chronic liver injury leads to liver inflammation and fibrosis (LF) as critical determinants of long-term outcomes such as cirrhosis, liver cancer, and mortality. LF is a wound-healing process characterized by excessive deposition of extracellular matrix (ECM) proteins due to the activation of hepatic stellate cells (HSCs). In the healthy liver, quiescent HSCs metabolize and store retinoids. Upon fibrogenic activation, quiescent HSCs transdifferentiate into myofibroblasts; lose their vitamin A; upregulate α-smooth muscle actin; and produce proinflammatory soluble mediators, collagens, and inhibitors of ECM degradation. Activated HSCs are the main effector cells during hepatic fibrogenesis. In addition, the accumulation and activation of profibrogenic macrophages in response to hepatocyte death play a critical role in the initiation of HSC activation and survival. The main source of myofibroblasts is resident HSCs. Activated HSCs migrate to the site of active fibrogenesis to initiate the formation of a fibrous scar. Single-cell technologies revealed that quiescent HSCs are highly homogenous, while activated HSCs/myofibroblasts are much more heterogeneous. The complex process of inflammation results from the response of various hepatic cells to hepatocellular death and inflammatory signals related to intrahepatic injury pathways or extrahepatic mediators. Inflammatory processes modulate fibrogenesis by activating HSCs and, in turn, drive immune mechanisms via cytokines and chemokines. Increasing evidence also suggests that cellular stress responses contribute to fibrogenesis. Recent data demonstrated that LF can revert even at advanced stages of cirrhosis if the underlying cause is eliminated, which inhibits the inflammatory and profibrogenic cells. However, despite numerous clinical studies on plausible drug candidates, an approved antifibrotic therapy still remains elusive. This state-of-the-art review presents cellular and molecular mechanisms involved in hepatic fibrogenesis and its resolution, as well as comprehensively discusses the drivers linking liver injury to chronic liver inflammation and LF. Full article
(This article belongs to the Special Issue Molecular Advances in Liver Fibrosis)
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25 pages, 1805 KiB  
Review
Can Nutraceuticals Support the Treatment of MASLD/MASH, and thus Affect the Process of Liver Fibrosis?
by Aneta Sokal-Dembowska, Sara Jarmakiewicz-Czaja, Katarzyna Ferenc and Rafał Filip
Int. J. Mol. Sci. 2024, 25(10), 5238; https://doi.org/10.3390/ijms25105238 - 11 May 2024
Cited by 5 | Viewed by 2054
Abstract
Currently, metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are considered to be the main causes of fibrosis. In turn, fibrosis may lead to the development of hepatocellular carcinoma or advanced cirrhosis, i.e., potentially life-threatening conditions. It is likely that [...] Read more.
Currently, metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are considered to be the main causes of fibrosis. In turn, fibrosis may lead to the development of hepatocellular carcinoma or advanced cirrhosis, i.e., potentially life-threatening conditions. It is likely that therapy aimed at reducing the risk of developing hepatic steatosis and inflammation could be helpful in minimizing the threat/probability of organ fibrosis. In recent years, increasing attention has been paid to the influence of nutraceuticals in the prevention and treatment of liver diseases. Therefore, the aim of this review was to describe the precise role of selected ingredients such as vitamin C, beta-carotene, omega-3 fatty acids, and curcumin. It is likely that the use of these ingredients in the treatment of patients with MASLD/MASH, along with behavioral and pharmacological therapy, may have a beneficial effect on combating inflammation, reducing oxidative stress, and thereby preventing liver damage. Full article
(This article belongs to the Special Issue Molecular Advances in Liver Fibrosis)
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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 3 | Viewed by 1555
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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