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Antioxidants
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Cellular and Molecular Regulation of Genomic and Epigenetic Integrity by...
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Cellular and Molecular Regulation of Genomic and Epigenetic Integrity by ROS/RNS

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 7769

Special Issue Editors

Prof. Dr. Mark G. Clemens

E-Mail Website
Guest Editor
Center for Biomedical Science and Engineering, University of North Carolina at Charlotte, Charlotte, NC 28223, USA
Interests: nitric oxide; ischemia/reperfusion; inflammation; DNA damage/repair; hydrogen sulfide; liver; microcirculation
Special Issues, Collections and Topics in MDPI journals
Dr. Shan Yan

E-Mail Website
Guest Editor
University of North Carolina at Charlotte, USA
Interests: DNA damage; DNA repair; DNA damage response; cancer etiology; environmental health; genome integrity; oxidative stress; Xenopus laevis

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) may have both beneficial and harmful roles in cell physiology and pathology. It is important to elucidate how genome and epigenetic integrity are maintained in the cellular and molecular responses to ROS/RNS. Within cells, ROS/RNS may affect macromolecules, including nucleic acids (DNA/RNA), proteins, and lipids. At the level of genome integrity, DNA lesions induced by ROS/RNS can be repaired by a variety of different DNA repair and DNA damage response pathways. At the level of epigenetic regulation, ROS/RNS may induce or regulate the gene expression of certain stress response pathways that, in turn can protect against subsequent stresses. Conversely, excessive or poorly regulated activation can lead to potentiation of inflammation and be counter-regulatory. As such, these regulatory mechanisms not only change nuclear and mitochondria functions within the cells but also affect the functionalities of tissues and organs.

Both review articles and original research articles within this area of research are welcome to submit in response to this Special Issue. We will also send invitations to active researchers in this area.

Prof. Dr. Mark G. Clemens
Dr. Shan Yan
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

  • Genomic integrity
  • Epigenetic integrity and regulation
  • ROS/RNS
  • Inflammation
  • DNA damage response

Published Papers (2 papers)

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Review

18 pages, 1135 KiB  
Review
Sirtuins and Sepsis: Cross Talk between Redox and Epigenetic Pathways
by Anugraha Gandhirajan, Sanjoy Roychowdhury and Vidula Vachharajani
Antioxidants 2022, 11(1), 3; https://doi.org/10.3390/antiox11010003 - 21 Dec 2021
Cited by 7 | Viewed by 3100
Abstract
Sepsis and septic shock are the leading causes of death among hospitalized patients in the US. The immune response in sepsis transitions from a pro-inflammatory and pro-oxidant hyper-inflammation to an anti-inflammatory and cytoprotective hypo-inflammatory phase. While 1/3rd sepsis-related deaths occur during hyper-, a [...] Read more.
Sepsis and septic shock are the leading causes of death among hospitalized patients in the US. The immune response in sepsis transitions from a pro-inflammatory and pro-oxidant hyper-inflammation to an anti-inflammatory and cytoprotective hypo-inflammatory phase. While 1/3rd sepsis-related deaths occur during hyper-, a vast majority of sepsis-mortality occurs during the hypo-inflammation. Hyper-inflammation is cytotoxic for the immune cells and cannot be sustained. As a compensatory mechanism, the immune cells transition from cytotoxic hyper-inflammation to a cytoprotective hypo-inflammation with anti-inflammatory/immunosuppressive phase. However, the hypo-inflammation is associated with an inability to clear invading pathogens, leaving the host susceptible to secondary infections. Thus, the maladaptive immune response leads to a marked departure from homeostasis during sepsis-phases. The transition from hyper- to hypo-inflammation occurs via epigenetic programming. Sirtuins, a highly conserved family of histone deacetylators and guardians of homeostasis, are integral to the epigenetic programming in sepsis. Through their anti-inflammatory and anti-oxidant properties, the sirtuins modulate the immune response in sepsis. We review the role of sirtuins in orchestrating the interplay between the oxidative stress and epigenetic programming during sepsis. Full article
(This article belongs to the Special Issue Cellular and Molecular Regulation of Genomic and Epigenetic Integrity by ROS/RNS)
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21 pages, 1543 KiB  
Review
Mechanisms of Ataxia Telangiectasia Mutated (ATM) Control in the DNA Damage Response to Oxidative Stress, Epigenetic Regulation, and Persistent Innate Immune Suppression Following Sepsis
by Laura A. Huff, Shan Yan and Mark G. Clemens
Antioxidants 2021, 10(7), 1146; https://doi.org/10.3390/antiox10071146 - 20 Jul 2021
Cited by 8 | Viewed by 3922
Abstract
Cells have evolved extensive signaling mechanisms to maintain redox homeostasis. While basal levels of oxidants are critical for normal signaling, a tipping point is reached when the level of oxidant species exceed cellular antioxidant capabilities. Myriad pathological conditions are characterized by elevated oxidative [...] Read more.
Cells have evolved extensive signaling mechanisms to maintain redox homeostasis. While basal levels of oxidants are critical for normal signaling, a tipping point is reached when the level of oxidant species exceed cellular antioxidant capabilities. Myriad pathological conditions are characterized by elevated oxidative stress, which can cause alterations in cellular operations and damage to cellular components including nucleic acids. Maintenance of nuclear chromatin are critically important for host survival and eukaryotic organisms possess an elaborately orchestrated response to initiate repair of such DNA damage. Recent evidence indicates links between the cellular antioxidant response, the DNA damage response (DDR), and the epigenetic status of the cell under conditions of elevated oxidative stress. In this emerging model, the cellular response to excessive oxidants may include redox sensors that regulate both the DDR and an orchestrated change to the epigenome in a tightly controlled program that both protects and regulates the nuclear genome. Herein we use sepsis as a model of an inflammatory pathophysiological condition that results in elevated oxidative stress, upregulation of the DDR, and epigenetic reprogramming of hematopoietic stem cells (HSCs) to discuss new evidence for interplay between the antioxidant response, the DNA damage response, and epigenetic status. Full article
(This article belongs to the Special Issue Cellular and Molecular Regulation of Genomic and Epigenetic Integrity by ROS/RNS)
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