Special Issue "Mitochondria-Targeted Antioxidants"
A special issue of Antioxidants (ISSN 2076-3921).
Deadline for manuscript submissions: closed (15 April 2019)
Mitochondria are believed to be the main reactive oxygen species (ROS) source in a wide spectrum of diseases and pathologies, from cardiovascular conditions like stroke and myocardiac infarction to Parkinson’s disease, Alzheimer’s disease, diabetes, and even cancer. This makes them promising targets for pharmaceutical intervention. Furthermore, ROS are essential signaling molecules needed for normal cell physiology, while excessive amounts of ROS should be targeted and neutralized.
Mitochondria-targeted antioxidants provide one of the means to at least partially solve this problem. Since they are directed to the major site of cellular ROS production, their side effects on “signaling ROS” are noticeably reduced, and their therapeutic concentrations could be much lower than those of general antioxidants.
Recently, several types of mitochondria-targeted antioxidants have been developed. Many of them are permeable ions which carry a lipophilic delocalized positive charge, while others have an SS-type mitochondria-targeting peptide, and some use channel-forming compounds to permeabilize the mitochondrial membrane. An antioxidant moiety is also different among these substances: they can carry ROS-scavenging compounds, iron chelators, and mitochondria-targeted antioxidant enzymes such as catalase.
Mitochondria-targeted antioxidants have already been shown to bear a therapeutic effect on Parkinson's and Alzheimer's diseases, type 2 diabetes, hypertension, sepsis, acute bacterial infection as well as diseases caused by xenobiotics, toxic chemicals or irradiation. However, we still need to clarify a number of issues: Should we specifically target mitochondria or not? Do we want to target the mitochondrial matrix or the membrane? What principle of ROS neutralization should be used? Whether we should target chemical or signaling effect of ROS. The purpose of this Special Issue is to bring together our current knowledge of the impact of mitochondria-targeted antioxidants on treatment of different pathologies and diseases. We would like to highlight on the future perspectives and challenges for such antioxidants to overcome their limitations in clinical practice as one of the most universal and promising approaches for treatment of diseases without hiding their adverse effects.
The editors of this Special Issue invite researchers in the field to contribute original research papers and review articles on the subject to this ambitious task.
Prof. Dr. Dmitry B. Zorov
Prof. Dr. Egor Yu. Plotnikov
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 papers will be 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 550 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.
- reactive oxygen species
- oxidative stress