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Antioxidants
Special Issues
Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related
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Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 May 2024) | Viewed by 8883

Special Issue Editors

Dr. Angela Inácio

E-Mail Website
Guest Editor
Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
Interests: metabolic disease; diet; oxidative stress; epigenetics
Dr. Ana Paula Barbosa

E-Mail Website
Guest Editor
Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
Interests: metabolic bone disease; nutrition; osteoporosis
Dr. Alda Pereira Da Silva

E-Mail Website
Guest Editor
Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal
Interests: metabolic disease; nutrition; oxidative metabolism; cardiovascular diseases
Dr. Marco G. Alves

E-Mail Website
Guest Editor
Institute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, 3810-193 Aveiro, Portugal
Interests: metabolism; mitochondria; omics; andrology; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic diseases are diseases or disorders that disrupt physiological metabolism. Usually, they promote alterations that are reflected in the accumulation or deficiency of certain metabolite(s). Those diseases can be classified as inherited metabolic disorders or acquired metabolic disorders. Inherited disorders are associated with inborn errors of metabolism, caused by genetic defects normally affecting specific enzymes or a group of enzymes' normal function. Acquired disorders are associated with environmental factors, usually lifestyle-related, such as physical activity or caloric intake. Indeed, human lifestyle is an important player in the onset of these diseases and has been associated with the inherited epigenetic pattern, that affects the expression, of genes encoding for important proteins of the metabolism homeostasis.

Metabolism is markedly linked to oxidative stress which is a hallmark of all modern diseases, and metabolic diseases are no exception. Cardiovascular diseases, hypertension, diabetes mellitus, insulin resistance, osteoporosis and obesity, are common chronic diseases where certain conditions such as hyperglycemia, hypercholesterolemia, hypertriglyceridemia, inflammation, neurotoxicity, and genomic instability are present. Oxidative stress damages cellular mechanisms and disturbs their function, contributing to the disease´s onset and/or progression. In order to acquire a good balance between oxidative and antioxidative processes, lifestyle options, including exercise and an appropriate intake of nutritional antioxidants (flavonoids, arginine, vitamin C, vitamin E, carotenoids, resveratrol, and selenium) might be important to improve or avoid oxidative stress-related effects. Expanding the knowledge on how oxidative stress influences the development of metabolic disorders may help to implement new nutritional and pharmaceutical strategies to improve the outcome.

Epigenetic factors have also emerged as pivotal factors in the onset and development of metabolic diseases. On one hand, several studies report the potentially harmful effects of metabolic disorders in the genetic and epigenetic cargo of germ and somatic cells. On the other hand, the inheritance of epigenetic factors towards the development of metabolic abnormalities means that metabolic cues from the parents can be passed to the next generations. These mechanisms that mediate possible transgenerational effects of metabolic diseases and how oxidative stress is a player, remain largely unknown.

This Special Issue aims to provide a broad and updated overview of the involvement of “Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related”. We intend to shed some light on the subject, by sharing new clinical or basic studies using genome/epigenome-wide or target genetic/epigenetic approaches. We search for contributions by experts in the field in the form of research papers or critical reviews.

Dr. Angela Inácio
Dr. Ana Paula Barbosa
Dr. Alda Pereira Da Silva
Dr. Marco G. Alves
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. Antioxidants 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 2900 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

  • oxidative stress
  • genetics
  • epigenetics
  • alleles
  • epialleles
  • histone modifications
  • DNA methylation
  • small RNAs
  • inborn errors of metabolism
  • acquired metabolic disorders
  • genetic target approaches
  • genome wide approaches
  • pharmacogenetics
  • nutrigenomics
  • gametes

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Published Papers (4 papers)

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19 pages, 366 KiB  
Article
Genetic Modulation of HPV Infection and Cervical Lesions: Role of Oxidative Stress-Related Genes
by Ângela Inácio, Laura Aguiar, Beatriz Rodrigues, Patrícia Pires, Joana Ferreira, Andreia Matos, Inês Mendonça, Raquel Rosa, Manuel Bicho, Rui Medeiros and Maria Clara Bicho
Antioxidants 2023, 12(10), 1806; https://doi.org/10.3390/antiox12101806 - 27 Sep 2023
Cited by 4 | Viewed by 1545
Abstract
Human papillomavirus (HPV) infection is a necessary but not sufficient factor for the development of invasive cervical cancer (ICC) and high-grade intraepithelial lesion (HSIL). Oxidative stress is known to play a crucial role in HPV infection and carcinogenesis. In this study, we comprehensively [...] Read more.
Human papillomavirus (HPV) infection is a necessary but not sufficient factor for the development of invasive cervical cancer (ICC) and high-grade intraepithelial lesion (HSIL). Oxidative stress is known to play a crucial role in HPV infection and carcinogenesis. In this study, we comprehensively investigate the modulation of HPV infection, HSIL and ICC, and ICC through an exploration of oxidative stress-related genes: CβS, MTHFR, NOS3, ACE1, CYBA, HAP, ACP1, GSTT1, GSTM1, and CYP1A1. Notably, the ACE1 gene emerges as a prominent factor with the presence of the I allele offering protection against HPV infection. The association of NOS3 with HPV infection is perceived with the 4a allele showing a protective effect. The presence of the GSTT1 null mutant correlates with increased susceptibility to HPV infection, HSIL and ICC, and ICC. This study also uncovers intriguing epistatic interactions among some of the genes that further accentuate their roles in disease modulation. Indeed, the epistatic interactions between the BB genotype (ACP1) and DD genotype (ECA1) were shown to increase the risk of HPV infection, and the interaction between BB (ACP1) and 0.0 (GSTT1) was associated with HPV infection and cervical lesions. These findings underscore the pivotal role of four oxidative stress-related genes in HPV-associated cervical lesions and cancer development, enriching our clinical understanding of the genetic influences on disease manifestation. The awareness of these genetic variations holds potential clinical implications. Full article
(This article belongs to the Special Issue Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related)
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Review

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20 pages, 1523 KiB  
Review
Tricarboxylic Acid Cycle Regulation of Metabolic Program, Redox System, and Epigenetic Remodeling for Bone Health and Disease
by Wei-Shiung Lian, Re-Wen Wu, Yu-Han Lin, Yu-Shan Chen, Holger Jahr and Feng-Sheng Wang
Antioxidants 2024, 13(4), 470; https://doi.org/10.3390/antiox13040470 - 17 Apr 2024
Cited by 2 | Viewed by 1982
Abstract
Imbalanced osteogenic cell-mediated bone gain and osteoclastic remodeling accelerates the development of osteoporosis, which is the leading risk factor of disability in the elderly. Harmonizing the metabolic actions of bone-making cells and bone resorbing cells to the mineralized matrix network is required to [...] Read more.
Imbalanced osteogenic cell-mediated bone gain and osteoclastic remodeling accelerates the development of osteoporosis, which is the leading risk factor of disability in the elderly. Harmonizing the metabolic actions of bone-making cells and bone resorbing cells to the mineralized matrix network is required to maintain bone mass homeostasis. The tricarboxylic acid (TCA) cycle in mitochondria is a crucial process for cellular energy production and redox homeostasis. The canonical actions of TCA cycle enzymes and intermediates are indispensable in oxidative phosphorylation and adenosine triphosphate (ATP) biosynthesis for osteogenic differentiation and osteoclast formation. Knockout mouse models identify these enzymes’ roles in bone mass and microarchitecture. In the noncanonical processes, the metabolites as a co-factor or a substrate involve epigenetic modification, including histone acetyltransferases, DNA demethylases, RNA m6A demethylases, and histone demethylases, which affect genomic stability or chromatin accessibility for cell metabolism and bone formation and resorption. The genetic manipulation of these epigenetic regulators or TCA cycle intermediate supplementation compromises age, estrogen deficiency, or inflammation-induced bone mass loss and microstructure deterioration. This review sheds light on the metabolic functions of the TCA cycle in terms of bone integrity and highlights the crosstalk of the TCA cycle and redox and epigenetic pathways in skeletal tissue metabolism and the intermediates as treatment options for delaying osteoporosis. Full article
(This article belongs to the Special Issue Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related)
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25 pages, 1764 KiB  
Review
From Stress to Sick(le) and Back Again–Oxidative/Antioxidant Mechanisms, Genetic Modulation, and Cerebrovascular Disease in Children with Sickle Cell Anemia
by Marisa Silva and Paula Faustino
Antioxidants 2023, 12(11), 1977; https://doi.org/10.3390/antiox12111977 - 7 Nov 2023
Cited by 2 | Viewed by 1917
Abstract
Sickle cell anemia (SCA) is a genetic disease caused by the homozygosity of the HBB:c.20A>T mutation, which results in the production of hemoglobin S (HbS). In hypoxic conditions, HbS suffers autoxidation and polymerizes inside red blood cells, altering their morphology into a [...] Read more.
Sickle cell anemia (SCA) is a genetic disease caused by the homozygosity of the HBB:c.20A>T mutation, which results in the production of hemoglobin S (HbS). In hypoxic conditions, HbS suffers autoxidation and polymerizes inside red blood cells, altering their morphology into a sickle shape, with increased rigidity and fragility. This triggers complex pathophysiological mechanisms, including inflammation, cell adhesion, oxidative stress, and vaso-occlusion, along with metabolic alterations and endocrine complications. SCA is phenotypically heterogeneous due to the modulation of both environmental and genetic factors. Pediatric cerebrovascular disease (CVD), namely ischemic stroke and silent cerebral infarctions, is one of the most impactful manifestations. In this review, we highlight the role of oxidative stress in the pathophysiology of pediatric CVD. Since oxidative stress is an interdependent mechanism in vasculopathy, occurring alongside (or as result of) endothelial dysfunction, cell adhesion, inflammation, chronic hemolysis, ischemia-reperfusion injury, and vaso-occlusion, a brief overview of the main mechanisms involved is included. Moreover, the genetic modulation of CVD in SCA is discussed. The knowledge of the intricate network of altered mechanisms in SCA, and how it is affected by different genetic factors, is fundamental for the identification of potential therapeutic targets, drug development, and patient-specific treatment alternatives. Full article
(This article belongs to the Special Issue Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related)
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20 pages, 1060 KiB  
Review
Insights into the Role of Plasmatic and Exosomal microRNAs in Oxidative Stress-Related Metabolic Diseases
by Ayauly Duisenbek, Gabriela C. Lopez-Armas, Miguel Pérez, María D. Avilés Pérez, José Miguel Aguilar Benitez, Víctor Roger Pereira Pérez, Juan Gorts Ortega, Arailym Yessenbekova, Nurzhanyat Ablaikhanova, Germaine Escames, Darío Acuña-Castroviejo and Iryna Rusanova
Antioxidants 2023, 12(6), 1290; https://doi.org/10.3390/antiox12061290 - 16 Jun 2023
Cited by 7 | Viewed by 2406
Abstract
A common denominator of metabolic diseases, including type 2 diabetes Mellitus, dyslipidemia, and atherosclerosis, are elevated oxidative stress and chronic inflammation. These complex, multi-factorial diseases are caused by the detrimental interaction between the individual genetic background and multiple environmental stimuli. The cells, including [...] Read more.
A common denominator of metabolic diseases, including type 2 diabetes Mellitus, dyslipidemia, and atherosclerosis, are elevated oxidative stress and chronic inflammation. These complex, multi-factorial diseases are caused by the detrimental interaction between the individual genetic background and multiple environmental stimuli. The cells, including the endothelial ones, acquire a preactivated phenotype and metabolic memory, exhibiting increased oxidative stress, inflammatory gene expression, endothelial vascular activation, and prothrombotic events, leading to vascular complications. There are different pathways involved in the pathogenesis of metabolic diseases, and increased knowledge suggests a role of the activation of the NF-kB pathway and NLRP3 inflammasome as key mediators of metabolic inflammation. Epigenetic-wide associated studies provide new insight into the role of microRNAs in the phenomenon of metabolic memory and the development consequences of vessel damage. In this review, we will focus on the microRNAs related to the control of anti-oxidative enzymes, as well as microRNAs related to the control of mitochondrial functions and inflammation. The objective is the search for new therapeutic targets to improve the functioning of mitochondria and reduce oxidative stress and inflammation, despite the acquired metabolic memory. Full article
(This article belongs to the Special Issue Genetics and Epigenetic Modifications on Metabolic Diseases Oxidative Related)
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