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Liver Disease: Genetic Research and Clinical Diagnosis
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Liver Disease: Genetic Research and Clinical Diagnosis

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 10469

Special Issue Editors

Dr. Prasanna Kumar Santhekadur

E-Mail Website
Guest Editor
JSS Medical College & Hospital, Mysore 570015, India
Interests: liver disease; hepatocellular carcinoma (HCC); NAFLD; AFLD; nutrition; pharmacotherapy
Dr. Senthilkumar Rajagopal

E-Mail Website
Co-Guest Editor
Department of Biotechnology, REVA University, Bengaluru 560064, India
Interests: biochemistry; physiology cancer; immunology; anesthesiology; molecular biology

Special Issue Information

Dear Colleagues,

The liver is one of the most vital and largest organs of the human body. Recently, due to a changed lifestyle, a huge consumption of a high calorie diet and westernisation, there are rapidly increased incidences of chronic liver disease. Understanding the progression and molecular mechanism of chronic liver disease is important in today’s society. There are many cutting-edge research studies that are in progress to help us understand these life-threatening maladies across the globe. In this Special Issue, we are soliciting all types of research papers and review articles which deal with recent advances in liver diseases, including NAFLD, AFLD, HCC, virus-associated hepatitis, and drug-induced liver disease.

Dr. Prasanna Kumar Santhekadur
Dr. Senthilkumar Rajagopal
Guest Editors

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. Genes 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 2600 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

  • hepatocellular carcinoma
  • nonalcoholic fatty liver disease
  • alcoholic fatty liver disease
  • hepatitis

Published Papers (5 papers)

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Research

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10 pages, 2679 KiB  
Article
Novel Insights into MEG3/miR664a-3p/ADH4 Axis and Its Possible Role in Hepatocellular Carcinoma from an in Silico Perspective
by Shreyas H. Karunakara, Lakshana D. Puttahanumantharayappa, Nirmala G. Sannappa Gowda, Varsha D. Shiragannavar and Prasanna K. Santhekadur
Genes 2022, 13(12), 2254; https://doi.org/10.3390/genes13122254 - 30 Nov 2022
Cited by 3 | Viewed by 1609
Abstract
Hepatocellular carcinoma (HCC) is a complex disease involving altered interactomes of transcripts and proteins. MicroRNAs (miRNAs) are small-noncoding RNAs that can interact with specific gene transcripts and an array of other vital endogenous non-coding RNAs (lncRNAs) that can influence gene expression. Maternally Expressed [...] Read more.
Hepatocellular carcinoma (HCC) is a complex disease involving altered interactomes of transcripts and proteins. MicroRNAs (miRNAs) are small-noncoding RNAs that can interact with specific gene transcripts and an array of other vital endogenous non-coding RNAs (lncRNAs) that can influence gene expression. Maternally Expressed Gene 3 (MEG3) is an imprinted lncRNA that is reported to be downregulated in HCC (in both cell lines and tumors). Alcohol Dehydrogenase 4 (ADH4) is a well-known prognostic protein biomarker for predicting the survival outcomes of patients with hepatocellular carcinoma whose expression is regulated by miR-664a-3p, which is upregulated in HCC. In this study, we performed a battery of robust and systematic in silico analyses to predicate the possible lncRNA–miRNA interactions between MEG3, miR-664a-3p, and ADH4. miRNA–mRNA and lncRNA–miRNA hybrid structures were primarily obtained, and the minimum free energies (MFEs) for the 3′UTR (Untranslated Regions) of ADH4-miR-664a-3p and the 3′UTR of MEG3-miR-664a-3p interactions were assessed to predict the stability of the obtained RNA heteroduplex hybrids. The hybrid with the least minimum free energy (MFE) was considered to be the most favorable. The MFEs were around −28.1 kcal/mol and −31.3 kCal/mol for the ADH4-miR-664a-3p and MEG3-miR-66a-3p RNA hybrids, respectively. This demonstrated that lncRNA-MEG3 might be a competitive endogenous RNA that acts as a molecular sponge for miR-664a-3p. In summary, our interaction analyses results predict the significance of the MEG3/miR-664a-3p/ADH4 axis, where MEG3 downregulation results in miR-664a-3p overexpression and the subsequential underexpression of ADH4 in HCC, as a novel axis of interest that demands further validation. Full article
(This article belongs to the Special Issue Liver Disease: Genetic Research and Clinical Diagnosis)
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Review

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7 pages, 2968 KiB  
Review
Exercise Does Not Independently Improve Histological Outcomes in Biopsy-Proven Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis
by George Chen, Bubu A. Banini, Albert Do, Craig Gunderson, Saif Zaman and Joseph K. Lim
Genes 2023, 14(9), 1811; https://doi.org/10.3390/genes14091811 - 17 Sep 2023
Cited by 4 | Viewed by 1043
Abstract
Introduction: The independent effect of exercise on liver histology in non-alcoholic fatty liver disease (NAFLD) remains unclear. As such, we conducted a systematic review and meta-analysis of the effect of exercise alone on histological endpoints in biopsy-proven NAFLD. Materials and Methods: A systematic [...] Read more.
Introduction: The independent effect of exercise on liver histology in non-alcoholic fatty liver disease (NAFLD) remains unclear. As such, we conducted a systematic review and meta-analysis of the effect of exercise alone on histological endpoints in biopsy-proven NAFLD. Materials and Methods: A systematic literature search was conducted to include controlled clinical trials investigating the effect of exercise alone on liver histology in biopsy-proven NAFLD. Meta-analysis was conducted for histological outcomes with available data from a minimum of three studies. Pooled estimates of the effect of exercise on histological endpoints were calculated using random-effects models. Results: We identified three controlled clinical trials that assessed the independent effect of exercise on histological outcomes in patients with biopsy-proven NAFLD. The studies consisted of 72 total participants, including 40 subjects in the exercise intervention and 32 individuals in the comparison group. Meta-analysis showed that exercise did not significantly improve Brunt grade, NAFLD activity score, and fibrosis in NAFLD. Discussion: Exercise alone may not lead to significant histopathological improvement in NAFLD. Future well-powered randomized controlled trials are needed to better characterize the impact of exercise on histological outcomes and clinical endpoints. Full article
(This article belongs to the Special Issue Liver Disease: Genetic Research and Clinical Diagnosis)
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15 pages, 790 KiB  
Review
Nanoplastics Toxicity Specific to Liver in Inducing Metabolic Dysfunction—A Comprehensive Review
by Shoumi Haldar, Nounenuo Yhome, Yuvashree Muralidaran, Senthilkumar Rajagopal and Prabhakar Mishra
Genes 2023, 14(3), 590; https://doi.org/10.3390/genes14030590 - 26 Feb 2023
Cited by 8 | Viewed by 2864
Abstract
Plastic pollution in the world is widespread and growing. The environment is swamped with nanoplastics (<100 nm), and the health consequences of these less visible pollutants are unknown. Furthermore, there is evidence that microplastics can release nanoplastics by digestive disintegration, implying that macroplastic [...] Read more.
Plastic pollution in the world is widespread and growing. The environment is swamped with nanoplastics (<100 nm), and the health consequences of these less visible pollutants are unknown. Furthermore, there is evidence that microplastics can release nanoplastics by digestive disintegration, implying that macroplastic exposure can cause direct and indirect disease via nanoplastics. The existence and impact of nanoplastics in numerous tissues from invertebrates to larger vertebrates that consume significant amounts of plastics were investigated, and histopathological techniques were utilized to determine physiological reactions and inflammation from the plastics. Nanoplastics enters an organism through the respiratory and gastro-intestinal tract where they accumulate into the liver through blood circulation via absorption, or epidermal infiltration. It is stated that macroplastics can cause damage directly at the site of exposure, whereas nanoplastics can influence the liver, causing subsequent damage to other organs. Multi-organ dysfunction is brought on by liver changes, and nanoplastics can readily enter the gut-liver axis and disturb the gut microflora. By exploring the literature and summarizing the research that has been published to date, this review article reveals the deleterious effect and mechanisms of nanoplastics on the pathophysiological functions of the hepatic system. Full article
(This article belongs to the Special Issue Liver Disease: Genetic Research and Clinical Diagnosis)
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13 pages, 762 KiB  
Review
Autophagy: A Cellular Guardian against Hepatic Lipotoxicity
by Rohit Anthony Sinha
Genes 2023, 14(3), 553; https://doi.org/10.3390/genes14030553 - 22 Feb 2023
Cited by 5 | Viewed by 2331
Abstract
Lipotoxicity is a phenomenon of lipid-induced cellular injury in nonadipose tissue. Excess of free saturated fatty acids (SFAs) contributes to hepatic injury in nonalcoholic fatty liver disease (NAFLD), which has been growing at an unprecedented rate in recent years. SFAs and their derivatives [...] Read more.
Lipotoxicity is a phenomenon of lipid-induced cellular injury in nonadipose tissue. Excess of free saturated fatty acids (SFAs) contributes to hepatic injury in nonalcoholic fatty liver disease (NAFLD), which has been growing at an unprecedented rate in recent years. SFAs and their derivatives such as ceramides and membrane phospholipids have been shown to induce intrahepatic oxidative damage and ER stress. Autophagy represents a cellular housekeeping mechanism to counter the perturbation in organelle function and activation of stress signals within the cell. Several aspects of autophagy, including lipid droplet assembly, lipophagy, mitophagy, redox signaling and ER-phagy, play a critical role in mounting a strong defense against lipotoxic lipid species within the hepatic cells. This review provides a succinct overview of our current understanding of autophagy–lipotoxicity interaction and its pharmacological and nonpharmacological modulation in treating NAFLD. Full article
(This article belongs to the Special Issue Liver Disease: Genetic Research and Clinical Diagnosis)
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Other

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13 pages, 604 KiB  
Project Report
A Comparative Study of Acute Alcoholic Hepatitis vs. Non-Alcoholic Hepatitis Patients from a Cohort with Chronic Alcohol Dependence
by Kyaw Min Tun, Zahra Dossaji, Blaine L. Massey, Kavita Batra, Chun-Han Lo, Yassin Naga, Salman Mohammed, Abebe Muraga, Ahmad Gill, Dwaipayan Mukhopadhyay, Ashok Singh, Daisy Lankarani, Jose Aponte-Pieras and Gordon Ohning
Genes 2023, 14(4), 780; https://doi.org/10.3390/genes14040780 - 23 Mar 2023
Cited by 2 | Viewed by 1841
Abstract
The rate of alcoholic hepatitis (AH) has risen in recent years. AH can cause as much as 40–50% mortality in severe cases. Successful abstinence has been the only therapy associated with long-term survival in patients with AH. Thus, it is crucial to be [...] Read more.
The rate of alcoholic hepatitis (AH) has risen in recent years. AH can cause as much as 40–50% mortality in severe cases. Successful abstinence has been the only therapy associated with long-term survival in patients with AH. Thus, it is crucial to be able to identify at-risk individuals in order to implement preventative measures. From the patient database, adult patients (age 18 and above) with AH were identified using the ICD-10 classification from November 2017 to October 2019. Liver biopsies are not routinely performed at our institution. Therefore, patients were diagnosed with AH based on clinical parameters and were divided into “probable” and “possible” AH. Logistic regression analysis was performed to determine risk factors associated with AH. A sub-analysis was performed to determine variables associated with mortality in AH patients. Among the 192 patients with alcohol dependence, there were 100 patients with AH and 92 patients without AH. The mean age was 49.3 years in the AH cohort, compared to 54.5 years in the non-AH cohort. Binge drinking (OR 2.698; 95% CI 1.079, 6.745; p = 0.03), heavy drinking (OR 3.169; 95% CI 1.348, 7.452; p = 0.01), and the presence of cirrhosis (OR 3.392; 95% CI 1.306, 8.811; p = 0.01) were identified as characteristics more commonly found in the AH cohort. Further, a higher inpatient mortality was seen in those with a probable AH diagnosis (OR 6.79; 95% CI 1.38, 44.9; p = 0.03) and hypertension (OR 6.51; 95% CI 9.49, 35.7; p = 0.02). A higher incidence of mortality was also noted among the non-Caucasian race (OR 2.72; 95% CI 4.92; 22.3; p = 0.29). A higher mortality rate despite a lower incidence of alcohol use among non-Caucasian patients may indicate healthcare disparities. Full article
(This article belongs to the Special Issue Liver Disease: Genetic Research and Clinical Diagnosis)
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