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Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment
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Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 14437

Special Issue Editor

Dr. Haibo Dong

E-Mail Website
Guest Editor
Center for Translational Biomedical Research, University of North Carolina at Greensboro, North Carolina Research Campus, Kannapolis, NC 28081, USA
Interests: fatty liver diseases; cellular redox balance; cell death; inflammation; oxidative stress; autophagy; mitochondrial dysfunction; NAD+ homeostasis

Special Issue Information

Dear Colleagues,

We are pleased to announce the call for papers for a Special Issue in Current Issues in Molecular Biology focused on exploring the cellular and molecular mechanisms that are involved in the development and progression of both non-alcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD).

NAFLD and ALD are significant contributors to the global burden of liver disease. NAFLD, often associated with metabolic syndrome, obesity, diabetes, and cardiovascular disease, has emerged as the most common cause of chronic liver disease worldwide. ALD, on the other hand, is primarily caused by excessive alcohol consumption and encompasses a wide range of liver conditions, including steatosis, alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. NAFLD and ALD are both steatohepatitic processes and share several common features, yet they are different in many aspects. Therefore, understanding the development and progression of both NAFLD and ALD, in addition to uncovering the underlying cellular and molecular mechanisms, is crucial to advancing our knowledge and developing effective therapeutic strategies for treating these liver diseases.

In this Special Issue, we welcome articles that investigate or summarize the cellular and molecular mechanisms that contribute to the pathogenesis and progression of NAFLD, NASH, ALD, and related diseases. We encourage researchers to explore a broad range of topics, including, but not limited to, impaired lipid metabolism, inflammation, oxidative stress, insulin resistance, genetic/epigenetic modifications, and the interplay between alcohol metabolism and liver injury.

Dr. Haibo Dong
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. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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

  • non-alcoholic fatty liver disease (NAFLD)
  • alcohol-associated liver disease (ALD)
  • lipotoxicity
  • bile acid metabolism
  • novel biomarker identification
  • organelle dysfunction and communication
  • inflammation and oxidative stress
  • cell signaling and cell death pathways
  • lipid metabolism and dysregulation
  • epigenetic modifications (DNA/RNA/non-coding RNA)
  • therapeutic targets and interventions

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Published Papers (8 papers)

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Research

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13 pages, 2109 KiB  
Article
The Effects of Warm Acupuncture on the Expression of AMPK in High-Fat Diet-Induced MAFLD Rats
by Yumi Lee, Donghee Choi, Junghye Park, Jae Gwan Kim, Taejin Choi and Daehwan Youn
Curr. Issues Mol. Biol. 2024, 46(10), 11580-11592; https://doi.org/10.3390/cimb46100687 - 17 Oct 2024
Viewed by 585
Abstract
This study investigated the effects of acupuncture and warm acupuncture on the expression and mechanism of the AMP-activated protein kinase (AMPK) signalling pathway associated with lipid accumulation in the liver tissue of rats with metabolic dysfunction-associated fatty liver disease (MAFLD) induced [...] Read more.
This study investigated the effects of acupuncture and warm acupuncture on the expression and mechanism of the AMP-activated protein kinase (AMPK) signalling pathway associated with lipid accumulation in the liver tissue of rats with metabolic dysfunction-associated fatty liver disease (MAFLD) induced by a high-fat diet. Sprague–Dawley rats were categorised into four groups: control (CON), untreated MAFLD (MAFLD), and two MAFLD groups treated with acupuncture (ACU) and warm acupuncture (WA). The treatment groups underwent 16 application sessions over 8 weeks at the SP9 and BL18 acupoints. We measured the expression levels of AMPK, sterol regulatory element-binding protein1 (SREBP1), acetyl-coenzyme A carboxylase (ACC), peroxisome proliferator-activated receptorα (PPARα), carnitine palmitoyltransferase1 (CPT1), and CPT2. AMPK was activated in both ACU and WA groups. WA downregulated both SREBP1 and ACC expression at the protein level, whereas the acupuncture treatment downregulated SREBP1 expression. Additionally, WA selectively induced the activation of signalling pathways related to AMPK, PPARα, CPT1, and CPT2 at the mRNA level. Histological observations confirmed that fat accumulation was reduced in both the ACU and the WA groups compared to the MAFLD group. The WA treatment-promoted amelioration of HFD-induced MAFLD may be related to the activation of the AMPK/SREBP1/ACC pathway in the liver. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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12 pages, 1798 KiB  
Article
Dimethyloxalylglycine Suppresses SREBP1c and Lipogenic Gene Expressions in Hepatocytes Independently of HIF1A
by Yong Seong Kwon, Ye Eun Cho, Yeonsoo Kim, Minseob Koh and Seonghwan Hwang
Curr. Issues Mol. Biol. 2024, 46(3), 2386-2397; https://doi.org/10.3390/cimb46030151 - 13 Mar 2024
Viewed by 1466
Abstract
Dimethyloxalylglycine (DMOG) is a representative inhibitor of the prolyl hydroxylase domain (PHD), which mediates the degradation of hypoxia-inducible factor-1-alpha (HIF1A). DMOG exerts its pharmacological effects via the canonical pathway that involves PHD inhibition; however, it remains unclear whether DMOG affects lipogenic gene expression [...] Read more.
Dimethyloxalylglycine (DMOG) is a representative inhibitor of the prolyl hydroxylase domain (PHD), which mediates the degradation of hypoxia-inducible factor-1-alpha (HIF1A). DMOG exerts its pharmacological effects via the canonical pathway that involves PHD inhibition; however, it remains unclear whether DMOG affects lipogenic gene expression in hepatocytes. We aimed to elucidate the effects of DMOG on sterol regulatory element-binding protein-1c (SREBP1c), a master regulator of fatty acid synthesis in hepatocytes. DMOG treatment inhibited SREBP1c mRNA and protein expression in HepG2 and AML12 hepatocytes and reduced the transcript levels of SREBP1c-regulated lipogenic genes. A luciferase reporter assay revealed that DMOG inhibited the transcriptional activity of SREBP1c. Moreover, DMOG suppressed SREBP1c expression in mice liver. Mechanistically, treatment with DMOG enhanced the expression of HIF1A and insulin-induced gene 2 (INSIG2), which inhibits the activation of SREBP1c. However, HIF1A or INSIG2 knockdown failed to reverse the inhibitory effect of DMOG on SREBP1c expression, suggesting a redundant role of HIF1A and INSIG2 in terms of repressing SREBP1c. DMOG did not function through the canonical pathway involving inhibition of SREBP1c by PHD, highlighting the presence of non-canonical pathways that mediate its anti-lipogenic effect. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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13 pages, 4044 KiB  
Article
Assessment of the (Pro)renin Receptor Protein Expression in Organs
by Teng-Yao Yang, Pey-Jium Chang, Yu-Shien Ko, Siou-Ru Shen and Shun-Fu Chang
Curr. Issues Mol. Biol. 2024, 46(3), 1741-1753; https://doi.org/10.3390/cimb46030113 - 25 Feb 2024
Cited by 1 | Viewed by 1180
Abstract
The (pro)renin receptor ((P)RR) is an essential component of the renin–angiotensin system (RAS) as a specific single-pass transmembrane receptor for prorenin and renin and has now emerged as a multifunctional protein implicated in a wide variety of developmental and physio-pathological processes and pathways. [...] Read more.
The (pro)renin receptor ((P)RR) is an essential component of the renin–angiotensin system (RAS) as a specific single-pass transmembrane receptor for prorenin and renin and has now emerged as a multifunctional protein implicated in a wide variety of developmental and physio-pathological processes and pathways. The (P)RR may be of pathological significance in metabolic syndrome. The (P)RR has received much consideration; substantial efforts have been made to understand the localization, regulation, and function of the (P)RR at both a molecular and system level. (P)RR regulation of cell function depends on whether it is intact or cleaved into its constituent forms. Therefore, the present chapter describes immunohistochemical approaches to examine the expression of (P)RR in various organs. It was shown that different molecular forms of (P)RR could be present in different tissue compartments in almost all organs. Among them, the liver has high PRR activity. Our findings could elucidate more detailed distribution of different (P)RR molecular forms in different organs, which could provide useful information to further investigate the pathophysiological mechanisms of the development of various diseases in the future. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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Review

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18 pages, 2003 KiB  
Review
Dual Roles of microRNA-122 in Hepatocellular Carcinoma and Breast Cancer Progression and Metastasis: A Comprehensive Review
by Essam Al Ageeli
Curr. Issues Mol. Biol. 2024, 46(11), 11975-11992; https://doi.org/10.3390/cimb46110711 - 25 Oct 2024
Viewed by 960
Abstract
microRNA-122 (miR-122) plays crucial yet contrasting roles in hepatocellular carcinoma (HCC) and breast cancer (BC), two prevalent and aggressive malignancies. This review synthesizes current research on miR-122’s functions in these cancers, focusing on its potential as a diagnostic, prognostic, and therapeutic target. A [...] Read more.
microRNA-122 (miR-122) plays crucial yet contrasting roles in hepatocellular carcinoma (HCC) and breast cancer (BC), two prevalent and aggressive malignancies. This review synthesizes current research on miR-122’s functions in these cancers, focusing on its potential as a diagnostic, prognostic, and therapeutic target. A comprehensive literature search was conducted using PubMed, Web of Science, and Scopus databases. In HCC, miR-122 is downregulated in most cases, suppressing oncogenic pathways and reducing tumor growth and metastasis. Restoring miR-122 levels has shown promising therapeutic potential, increasing sensitivity to treatments like sorafenib. In contrast, in BC, miR-122 plays a pro-metastatic role, especially in triple-negative breast cancer (TNBC) and metastatic lesions. miR-122′s ability to influence key pathways, such as the Wnt/β-catenin and NF-κB pathways in HCC, and its role in enhancing the Warburg effect in BC underline its significance in cancer biology. miR-122, a key factor in breast cancer radioresistance, suppresses tumors in radiosensitive cells. Inhibiting miR-122 could reverse resistance and potentially overcome radiotherapy resistance. Given its context-dependent functions, miR-122 could serve as a potential therapeutic target, where restoring or inhibiting its expression may help in treating HCC and BC, respectively. The dual roles of miR-122 underscore its significance in cancer biology and its potential in precision medicine. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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13 pages, 1591 KiB  
Review
The Role of Microbiota-Related Co-Metabolites in MASLD Progression: A Narrative Review
by Maria Martin-Grau and Daniel Monleón
Curr. Issues Mol. Biol. 2024, 46(7), 6377-6389; https://doi.org/10.3390/cimb46070381 - 25 Jun 2024
Viewed by 1274
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a growing health concern due to its increasing prevalence worldwide. Metabolic homeostasis encompasses the stable internal conditions vital for efficient metabolism. This equilibrium extends to the intestinal microbiota, whose metabolic activities profoundly influence overall metabolic balance [...] Read more.
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a growing health concern due to its increasing prevalence worldwide. Metabolic homeostasis encompasses the stable internal conditions vital for efficient metabolism. This equilibrium extends to the intestinal microbiota, whose metabolic activities profoundly influence overall metabolic balance and organ health. The metabolites derived from the gut microbiota metabolism can be defined as microbiota-related co-metabolites. They serve as mediators between the gut microbiota and the host, influencing various physiological processes. The recent redefinition of the term MASLD has highlighted the metabolic dysfunction that characterize the disease. Metabolic dysfunction encompasses a spectrum of abnormalities, including impaired glucose regulation, dyslipidemia, mitochondrial dysfunction, inflammation, and accumulation of toxic byproducts. In addition, MASLD progression has been linked to dysregulation in the gut microbiota and associated co-metabolites. Short-chain fatty acids (SCFAs), hippurate, indole derivatives, branched-chain amino acids (BCAAs), and bile acids (BAs) are among the key co-metabolites implicated in MASLD progression. In this review, we will unravel the relationship between the microbiota-related metabolites which have been associated with MASLD and that could play an important role for developing effective therapeutic interventions for MASLD and related metabolic disorders. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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18 pages, 676 KiB  
Review
Gut–Liver Axis as a Therapeutic Target for Drug-Induced Liver Injury
by Wenjing Tao, Qiwen Fan and Jintao Wei
Curr. Issues Mol. Biol. 2024, 46(2), 1219-1236; https://doi.org/10.3390/cimb46020078 - 1 Feb 2024
Cited by 3 | Viewed by 2371
Abstract
Drug-induced liver injury (DILI) is a liver disease that remains difficult to predict and diagnose, and the underlying mechanisms are yet to be fully clarified. The gut–liver axis refers to the reciprocal interactions between the gut and the liver, and its homeostasis plays [...] Read more.
Drug-induced liver injury (DILI) is a liver disease that remains difficult to predict and diagnose, and the underlying mechanisms are yet to be fully clarified. The gut–liver axis refers to the reciprocal interactions between the gut and the liver, and its homeostasis plays a prominent role in maintaining liver health. It has been recently reported that patients and animals with DILI have a disrupted gut–liver axis, involving altered gut microbiota composition, increased intestinal permeability and lipopolysaccharide translocation, decreased short-chain fatty acids production, and impaired bile acid metabolism homeostasis. The present review will summarize the evidence from both clinical and preclinical studies about the role of the gut–liver axis in the pathogenesis of DILI. Moreover, we will focus attention on the potential therapeutic strategies for DILI based on improving gut–liver axis function, including herbs and phytochemicals, probiotics, fecal microbial transplantation, postbiotics, bile acids, and Farnesoid X receptor agonists. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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17 pages, 9333 KiB  
Review
Recent Advances in Liver Tissue Engineering as an Alternative and Complementary Approach for Liver Transplantation
by Dileep G. Nair and Ralf Weiskirchen
Curr. Issues Mol. Biol. 2024, 46(1), 262-278; https://doi.org/10.3390/cimb46010018 - 29 Dec 2023
Cited by 3 | Viewed by 2771
Abstract
Acute and chronic liver diseases cause significant morbidity and mortality worldwide, affecting millions of people. Liver transplantation is the primary intervention method, replacing a non-functional liver with a functional one. However, the field of liver transplantation faces challenges such as donor shortage, postoperative [...] Read more.
Acute and chronic liver diseases cause significant morbidity and mortality worldwide, affecting millions of people. Liver transplantation is the primary intervention method, replacing a non-functional liver with a functional one. However, the field of liver transplantation faces challenges such as donor shortage, postoperative complications, immune rejection, and ethical problems. Consequently, there is an urgent need for alternative therapies that can complement traditional transplantation or serve as an alternative method. In this review, we explore the potential of liver tissue engineering as a supplementary approach to liver transplantation, offering benefits to patients with severe liver dysfunctions. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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19 pages, 1523 KiB  
Review
The Interconnection between Hepatic Insulin Resistance and Metabolic Dysfunction-Associated Steatotic Liver Disease—The Transition from an Adipocentric to Liver-Centric Approach
by Milena Vesković, Nikola Šutulović, Dragan Hrnčić, Olivera Stanojlović, Djuro Macut and Dušan Mladenović
Curr. Issues Mol. Biol. 2023, 45(11), 9084-9102; https://doi.org/10.3390/cimb45110570 - 14 Nov 2023
Cited by 17 | Viewed by 2844
Abstract
The central mechanism involved in the pathogenesis of MAFLD is insulin resistance with hyperinsulinemia, which stimulates triglyceride synthesis and accumulation in the liver. On the other side, triglyceride and free fatty acid accumulation in hepatocytes promotes insulin resistance via oxidative stress, endoplasmic reticulum [...] Read more.
The central mechanism involved in the pathogenesis of MAFLD is insulin resistance with hyperinsulinemia, which stimulates triglyceride synthesis and accumulation in the liver. On the other side, triglyceride and free fatty acid accumulation in hepatocytes promotes insulin resistance via oxidative stress, endoplasmic reticulum stress, lipotoxicity, and the increased secretion of hepatokines. Cytokines and adipokines cause insulin resistance, thus promoting lipolysis in adipose tissue and ectopic fat deposition in the muscles and liver. Free fatty acids along with cytokines and adipokines contribute to insulin resistance in the liver via the activation of numerous signaling pathways. The secretion of hepatokines, hormone-like proteins, primarily by hepatocytes is disturbed and impairs signaling pathways, causing metabolic dysregulation in the liver. ER stress and unfolded protein response play significant roles in insulin resistance aggravation through the activation of apoptosis, inflammatory response, and insulin signaling impairment mediated via IRE1/PERK/ATF6 signaling pathways and the upregulation of SREBP 1c. Circadian rhythm derangement and biological clock desynchronization are related to metabolic disorders, insulin resistance, and NAFLD, suggesting clock genes as a potential target for new therapeutic strategies. This review aims to summarize the mechanisms of hepatic insulin resistance involved in NAFLD development and progression. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying Fatty Liver Disease: From Pathogenesis to Treatment)
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