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Cells
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Cellular Mechanism and Interactions in Non-alcoholic Fatty Liver Disease
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Cellular Mechanism and Interactions in Non-alcoholic Fatty Liver Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 5741

Special Issue Editors

Dr. Rohit A. Sinha

E-Mail Website
Guest Editor
Sanjay Gandhi Postgraduate Institute of Medical Sciences Lucknow, Lucknow, India
Interests: NAFLD; autophagy; hormones
Dr. Mustapha Najimi

E-Mail Website
Guest Editor
Laboratory of Pediatric Hepatology and Cell Therapy, Institute of Experimental and Clinical Research (IREC), Université Catholique de Louvain, Louvain-la-Neuve, Belgium
Interests: liver cell therapy; mesenchymal stem cells; liver regeneration; hepatogenic differentiation; liver defects; cell therapy; liver cell types
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Non-alcoholic fatty liver disease (NAFLD), and more specifically its clinically relevant manifestation, non-alcoholic steatohepatitis (NASH), is a leading cause of liver transplant, type II diabetes, and hepatocellular cancer (HCC) in the world. Despite its growing incidence, both the diagnosis and treatment of NAFLD remain challenges. Recent studies have uncovered a plethora of cellular pathways involved in the crosstalk between hepatocytes and immune cells, which mediate the inflammation and progression of NAFLD to NASH in humans. Similarly, intracellular hormonal and cytokine action on hepatocytes regulates several facets of lipid metabolism, including lipogenesis, fat oxidation, and lipid droplet formation. Notably, lipotoxicity-mediated cellular stress and organelle damage have emerged as critical cellular events leading to NAFLD progression. Furthermore, damage-associated molecular patterns (DAMPs), composed of a combination of exogenous and endogenous danger signals, released by damaged hepatocytes result in the development and progression of sterile inflammation in NAFLD.  This Special Issue focuses on the cellular basis of NAFLD and its progression to NASH and NASH-HCC. Areas of interest include, but are not limited to, the roles of mitochondrial dysfunction, autophagy, oxidative stress, ER stress, and cytokines in the pathogenesis of NAFLD. This Special Issue aims to explore the intercellular interaction between liver cells and highlight the importance of targeting them as a novel therapeutic strategy for NAFLD treatment.

Dr. Rohit A. Sinha
Dr. Mustapha Najimi
Guest Editors

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Keywords

  • autophagy
  • inflammation
  • NASH
  • NAFLD
  • mitochondria
  • oxidative stress

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Published Papers (3 papers)

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Research

16 pages, 974 KiB  
Article
Non-Alcoholic Fatty Liver Disease Is Associated with a Decreased Catalase (CAT) Level, CT Genotypes and the T Allele of the -262 C/T CAT Polymorphism
by Marcin Kosmalski, Izabela Szymczak-Pajor, Józef Drzewoski and Agnieszka Śliwińska
Cells 2023, 12(18), 2228; https://doi.org/10.3390/cells12182228 - 7 Sep 2023
Cited by 4 | Viewed by 1375
Abstract
Background: It is well known that oxidative stress plays an important role in the development of non-alcoholic fatty liver disease (NAFLD). It has been suggested that an insufficient antioxidant defense system composed of antioxidant enzymes, including catalase (CAT) and nonenzymatic molecules, is a [...] Read more.
Background: It is well known that oxidative stress plays an important role in the development of non-alcoholic fatty liver disease (NAFLD). It has been suggested that an insufficient antioxidant defense system composed of antioxidant enzymes, including catalase (CAT) and nonenzymatic molecules, is a key factor triggering oxidative damage in the progression of liver disease. Therefore, the aim of our study was to assess whether the level of CAT and -262 C/T polymorphism in the promoter of CAT (rs1001179) are associated with NAFLD. Methods: In total, 281 adults (152/129 female/male, aged 65.61 ± 10.44 years) were included in the study. The patients were assigned to an NAFLD group (n = 139) or a group without NAFLD (n = 142) based on the results of an ultrasound, the Hepatic Steatosis Index, and the Fatty Liver Index (FLI). CAT levels were determined using an ELISA test, and genomic DNA was extracted via the standard phenol/chloroform-based method and genotyped via RFLP-PCR. Results: The CAT level was decreased in NAFLD patients (p < 0.001), and an ROC analysis revealed that a CAT level lower than 473.55 U/L significantly increases the risk of NAFLD. In turn, genotyping showed that the CT genotype and the T allele of -262 C/T CAT polymorphism elevate the risk of NAFLD. The diminished CAT level in the NAFLD group correlated with increased FLI, waist circumference and female gender. Conclusion: The obtained results support observations that oxidative damage associated with NAFLD may be the result of a decreased CAT level as a part of the antioxidant defense system. Full article
(This article belongs to the Special Issue Cellular Mechanism and Interactions in Non-alcoholic Fatty Liver Disease)
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13 pages, 3455 KiB  
Article
Targeting Extracellular RNA Mitigates Hepatic Lipotoxicity and Liver Injury in NASH
by Archana Tewari, Sangam Rajak, Sana Raza, Pratima Gupta, Bandana Chakravarti, Jyotika Srivastava, Chandra P. Chaturvedi and Rohit A. Sinha
Cells 2023, 12(14), 1845; https://doi.org/10.3390/cells12141845 - 13 Jul 2023
Cited by 2 | Viewed by 1664
Abstract
Non-alcoholic steatohepatitis (NASH) is a clinically serious stage of non-alcoholic fatty liver disease (NAFLD). Histologically characterized by hepatocyte ballooning, immune cell infiltration, and fibrosis, NASH, at a molecular level, involves lipid-induced hepatocyte death and cytokine production. Currently, there are very few diagnostic biomarkers [...] Read more.
Non-alcoholic steatohepatitis (NASH) is a clinically serious stage of non-alcoholic fatty liver disease (NAFLD). Histologically characterized by hepatocyte ballooning, immune cell infiltration, and fibrosis, NASH, at a molecular level, involves lipid-induced hepatocyte death and cytokine production. Currently, there are very few diagnostic biomarkers available to screen for NASH, and no pharmacological intervention is available for its treatment. In this study, we show that hepatocyte damage induced by lipotoxicity results in the release of extracellular RNAs (eRNAs), which serve as damage-associated molecular patterns (DAMPs) that stimulate the expression of pro-apoptotic and pro-inflammatory cytokines, aggravate inflammation, and lead to cell death in HepG2 cells. Furthermore, the inhibition of eRNA activity by RNase 1 significantly increases cellular viability and reduces NF-kB-mediated cytokine production. Similarly, RNase 1 administration significantly improves hepatic steatosis, inflammatory and injury markers in a murine NASH model. Therefore, this study, for the first time, underscores the therapeutic potential of inhibiting eRNA action as a novel strategy for NASH treatment. Full article
(This article belongs to the Special Issue Cellular Mechanism and Interactions in Non-alcoholic Fatty Liver Disease)
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18 pages, 4780 KiB  
Article
Fatty Acid Excess Dysregulates CARF to Initiate the Development of Hepatic Steatosis
by Kamrul M. Hasan, Meher Parveen, Alondra Pena, Francisco Bautista, Juan Carlos Rivera, Roxana Ramirez Huerta, Erica Martinez, Jorge Espinoza-Derout, Amiya P. Sinha-Hikim and Theodore C. Friedman
Cells 2023, 12(7), 1069; https://doi.org/10.3390/cells12071069 - 1 Apr 2023
Cited by 1 | Viewed by 2256
Abstract
CARF (CDKN2AIP) regulates cellular fate in response to various stresses. However, its role in metabolic stress is unknown. We found that fatty livers from mice exhibit low CARF expression. Similarly, overloaded palmitate inhibited CARF expression in HepG2 cells, suggesting that excess fat-induced stress [...] Read more.
CARF (CDKN2AIP) regulates cellular fate in response to various stresses. However, its role in metabolic stress is unknown. We found that fatty livers from mice exhibit low CARF expression. Similarly, overloaded palmitate inhibited CARF expression in HepG2 cells, suggesting that excess fat-induced stress downregulates hepatic CARF. In agreement with this, silencing and overexpressing CARF resulted in higher and lower fat accumulation in HepG2 cells, respectively. Furthermore, CARF overexpression lowered the ectopic palmitate accumulation in HepG2 cells. We were interested in understanding the role of hepatic CARF and underlying mechanisms in the development of NAFLD. Mechanistically, transcriptome analysis revealed that endoplasmic reticulum (ER) stress and oxidative stress pathway genes significantly altered in the absence of CARF. IRE1α, GRP78, and CHOP, markers of ER stress, were increased, and the treatment with TUDCA, an ER stress inhibitor, attenuated fat accumulation in CARF-deficient cells. Moreover, silencing CARF caused a reduction of GPX3 and TRXND3, leading to oxidative stress and apoptotic cell death. Intriguingly, CARF overexpression in HFD-fed mice significantly decreased hepatic steatosis. Furthermore, overexpression of CARF ameliorated the aberrant ER function and oxidative stress caused by fat accumulation. Our results further demonstrated that overexpression of CARF alleviates HFD-induced insulin resistance assessed with ITT and GTT assay. Altogether, we conclude that excess fat-induced reduction of CARF dysregulates ER functions and lipid metabolism leading to hepatic steatosis. Full article
(This article belongs to the Special Issue Cellular Mechanism and Interactions in Non-alcoholic Fatty Liver Disease)
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