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Cells
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Mitochondrial Functionality in Liver Pathologies
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Mitochondrial Functionality in Liver Pathologies

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

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 17428

Special Issue Editor

Dr. Matilde Bustos

E-Mail Website
Guest Editor
Institute of Biomedicine of Seville (IBiS). Spanish National Research Council (CSIC). University of Seville. Hospital Virgen del Rocio, Seville, Spain
Interests: liver disease; metabolism; mitochondria; non-alcoholic fatty liver disease; gp130 cytokines; inflammation

Special Issue Information

Dear Colleagues,

The incidence of chronic liver disease (CLD) and its end-stages, cirrhosis and liver cancer, are the leading causes of morbidity and mortality worldwide, with enormous socio-economic costs. The main causes of CLD are chronic viral hepatitis B or C infection, alcohol abuse, and obesity-linked steatohepatitis, conditions with increasing global incidence. Indeed, non-alcoholic fatty liver disease (NAFLD) is becoming the major cause of liver-related morbidity. Its prevalence is increasing worldwide, rising conjointly with obesity, insulin resistance, and cardiovascular risk. While the mechanisms behind the progression of liver disease have not been fully elucidated, mounting evidence suggests that oxidative stress and mitochondrial dysfunction are tightly linked to liver disease progression. Mitochondrial dysfunction is clearly implicated in exacerbating liver disease progression, and therapies that target the hepatic mitochondria may provide novel avenues for treatment. The aim of this Special Issue, titled “Mitochondrial Functionality in Liver Pathologies”, aims to provide compilation of literature evaluating the evidence behind the mitochondria alteration in the setting of liver disease and progression to fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Original research, systematic reviews, and meta-analyses should have a clear focus linking mitochondria and liver pathologies, prevention, progression, treatment, and/or reversion.

Dr. Matilde Bustos
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • liver diseases
  • progression of liver disease
  • liver cancer
  • metabolism
  • mitochondria
  • inflammation
  • oxidative stress

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Published Papers (3 papers)

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Research

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31 pages, 16978 KiB  
Article
Baicalein Activates Parkin-Dependent Mitophagy through NDP52 and OPTN
by Po-Yuan Ke, Chih-Wei Chang and Yuan-Chao Hsiao
Cells 2022, 11(7), 1132; https://doi.org/10.3390/cells11071132 - 28 Mar 2022
Cited by 8 | Viewed by 3976
Abstract
The elimination of intracellular components by autophagy maintains metabolic homeostasis and is a quality-control pathway that enables organelle regeneration. Mitophagy is a type of selective autophagy that regulates mitochondrial turnover, and the dysregulation of mitophagy has been implicated in the pathogenesis of liver [...] Read more.
The elimination of intracellular components by autophagy maintains metabolic homeostasis and is a quality-control pathway that enables organelle regeneration. Mitophagy is a type of selective autophagy that regulates mitochondrial turnover, and the dysregulation of mitophagy has been implicated in the pathogenesis of liver diseases. However, the detailed molecular mechanism underlying mitophagy regulation in liver cells remains unclear, and the small molecules that may potentially modulate hepatic mitophagy are still unavailable. Here, we report that baicalein, a flavonoid extracted from Scutellaria baicalensis, induces the entire autophagy that proceeds through the autolysosome maturation stage in human hepatoma cells. In addition, baicalein-induced autophagy is demonstrated to target mitochondria for degradation. Further studies show that baicalein triggers the translocation of Parkin and TBK1 to mitochondria to induce mitophagy. Moreover, the phosphorylation of TBK1 at Ser172 and ubiquitin at Ser65 is shown to trigger mitophagy in baicalein-treated cells. Furthermore, two specific autophagy cargo receptors, NDP52 and OPTN, that function in baicalein-activated mitophagy are identified. Taken together, these findings not only delineate the molecular process of Parkin-dependent mitophagy in liver cells, but also reveal baicalein as a novel inducer of hepatic mitophagy. Full article
(This article belongs to the Special Issue Mitochondrial Functionality in Liver Pathologies)
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16 pages, 3215 KiB  
Article
Hypertension and Aging Affect Liver Sulfur Metabolism in Rats
by Dominika Szlęzak, Patrycja Bronowicka-Adamska, Tomasz Hutsch, Marcin Ufnal and Maria Wróbel
Cells 2021, 10(5), 1238; https://doi.org/10.3390/cells10051238 - 18 May 2021
Cited by 16 | Viewed by 4769
Abstract
Hypertension and age are key risk factors for cardiovascular morbidity and mortality. Hydrogen sulfide (H2S), a gaseous transmitter, contributes significantly to regulating arterial blood pressure and aging processes. This study evaluated the effects of hypertension and aging on the hepatic metabolism [...] Read more.
Hypertension and age are key risk factors for cardiovascular morbidity and mortality. Hydrogen sulfide (H2S), a gaseous transmitter, contributes significantly to regulating arterial blood pressure and aging processes. This study evaluated the effects of hypertension and aging on the hepatic metabolism of sulfur-containing compounds, the activity of the enzymes involved in sulfur homeostasis, and the liver’s ability to generate H2S. Livers isolated from 16- and 60-week-old normotensive Wistar Kyoto rats (WKY) and Spontaneously Hypertensive Rats (SHR) were used to evaluate gene expression using RT-PCR, and the activity of enzymes participating in H2S metabolism, including thiosulfate sulfurtransferase (rhodanese; TST), cystathionine gamma-lyase (CTH), and 3-mercaptopyruvate sulfurtransferase (MPST). The levels of cysteine, cystine, reduced and oxidized glutathione were measured using RP-HPLC. SHR livers from both age groups showed a higher capacity to generate H2S than livers from WKY. The gene expression and activity of enzymes involved in sulfur metabolism differed between WKY and SHR, and between the age groups. For example, 16-week-old SHR had significantly higher activity of TST than 16-week-old WKY. Furthermore, differences between younger and older WKY rats in the expression and/or activity of TST and MPST were present. In conclusion, our study shows that arterial hypertension and aging affect hepatic sulfur metabolism and H2S production in rats. These findings pave the way for interventional studies evaluating a potential causal relation between liver sulfur metabolism, hypertension and aging. Full article
(This article belongs to the Special Issue Mitochondrial Functionality in Liver Pathologies)
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Review

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15 pages, 625 KiB  
Review
Mitochondrial Metabolic Signatures in Hepatocellular Carcinoma
by Ho-Yeop Lee, Ha Thi Nga, Jingwen Tian and Hyon-Seung Yi
Cells 2021, 10(8), 1901; https://doi.org/10.3390/cells10081901 - 27 Jul 2021
Cited by 62 | Viewed by 7936
Abstract
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide. HCC progression and metastasis are closely related to altered mitochondrial metabolism, including mitochondrial stress responses, metabolic reprogramming, and mitoribosomal defects. Mitochondrial oxidative phosphorylation (OXPHOS) defects and reactive oxygen species (ROS) [...] Read more.
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide. HCC progression and metastasis are closely related to altered mitochondrial metabolism, including mitochondrial stress responses, metabolic reprogramming, and mitoribosomal defects. Mitochondrial oxidative phosphorylation (OXPHOS) defects and reactive oxygen species (ROS) production are attributed to mitochondrial dysfunction. In response to oxidative stress caused by increased ROS production, misfolded or unfolded proteins can accumulate in the mitochondrial matrix, leading to initiation of the mitochondrial unfolded protein response (UPRmt). The mitokines FGF21 and GDF15 are upregulated during UPRmt and their levels are positively correlated with liver cancer development, progression, and metastasis. In addition, mitoribosome biogenesis is important for the regulation of mitochondrial respiration, cell viability, and differentiation. Mitoribosomal defects cause OXPHOS impairment, mitochondrial dysfunction, and increased production of ROS, which are associated with HCC progression in mouse models and human HCC patients. In this paper, we focus on the role of mitochondrial metabolic signatures in the development and progression of HCC. Furthermore, we provide a comprehensive review of cell autonomous and cell non-autonomous mitochondrial stress responses during HCC progression and metastasis. Full article
(This article belongs to the Special Issue Mitochondrial Functionality in Liver Pathologies)
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