DNA Damage and Repair in Degenerative Diseases 2016
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (31 March 2016) | Viewed by 146301
Special Issue Editor
Interests: oxidative stress-induced DNA damage and repair and its repair mechanisms in cardiometabolic and cancer diseases
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Damage to genetic material is the result of chemical changes and alterations that occur in the native sequence and conformational structure of DNA. The integrity of the genome is a compulsory hallmark, which much be maintained all along the development of biological organisms. This assumption is especially relevant considering the great amount endogenous and exogenous mechanisms that may compromise genomic stability and function of animal cells. One of the most, but not unique way of, damaging DNA or RNA is based on the production of reactive oxygen species (ROS) and subsequent oxidative modification. As a result of an oxidative stress insult to DNA, a number of damage bases are produced, adopting different molecular structures, some of which have been shown to induce mutagenesis. This is the case of the modified base 8-oxo-7,8-dihydro-2’-deoxyguanine (8-oxo-dG), an excellent indicator of oxidative stress with a promising future as a emergent tumor marker.
It its known that changes in the redox status of the cell have profound implication on the normal function of signal transduction pathways implicated in cell cycle regulation, which may lead to an abnormal cell proliferation and, eventually, cell-malignant transformation. In addition, highly reactive oxygen species, such as the hydroxyl radical (.OH), present great affinity towards DNA, and very easily interacts with its molecular structure to induce different degrees of oxidative modifications, which, depending on the intensity of their attack and impact, may range from single nucleotide oxidation to even the induction of double strands breaks. Recently, exposure to different environmental factors, such tobacco smoke or industry produced nanoparticles, have been shown to induce ROS as an endpoint mechanism, leading to nucleic acid oxidation and chronic inflammatory processes. Metal ion contamination is another way to induce DNA damage, by site-specific hydroxyl radical formation, via the well-known Fenton type reaction. However, there are many other interactive mechanisms which may also induce epigenetic DNA modifications, including adduct formation and addition of specific functional groups through acetylation and methylation reactions of chromatine proteins, with clear effects on their normal molecular processing.
Under normal metabolic conditions, the rate of DNA damage has been estimated at about 105 lesions/cell/day, which, although it represents a reduced proportion of the total genome, critical genes for the transcription of important signal transduction proteins may be affected, and, therefore, alter the normal homeostasis of cells and tissues. This may lead to an increase in the likelihood of genomic instability and the establishment of a broad spectrum of generative diseases, including cancer, neurodegeneration, inflammatory processes, and cardiovascular alterations, among many others. These facts emphasize the important role of DNA repair mechanisms in the preservation of the genome and in the prevention of physiological disturbances leading to disease. During the past few decades, it has been made clear that diminished repair efficiency plays an important role in the pathogenic scenario of degenerative diseases. An imbalance between repair and DNA damage eventually leads to an increase of gene mutations and malignant transformations of the cells. Therefore, impairments of specific DNA repair enzymes underlie the progression of many types of cancers, and knowledge of their molecular mechanisms has provided new tools for the development of advanced technologies allowing a much deeper understanding, diagnosis, and accurate treatment. Different types of DNA lesions accumulate in mammalian tissues with age and critical cell cycle check points with transcription and tumor suppressor function (p53, retinoblastoma, p16, p19, p21, etc.) play an important role in the control of cell proliferation, differentiation, and/or senescence and aging. The purpose of this Special Issue is to collect and offer, to the readers and researchers, recent highlights and advances on the regulatory mechanisms involved in DNA damage and repair, and their clinical implications with respect to widespread, related degenerative diseases.
Prof. Guillermo T. Sáez
Guest Editor
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Keywords
- DNA damage
- DNA repair
- 8-oxo-Dg
- aging
- degenerative diseases
- antioxidants signal transduction
- oxidative stress
- byproducts
- cardiovascular
- neurogeneration
- cancer
- metabolic diseases
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