IMR Press / JIN / Special Issues / mitochondrial_brain_neuro

Modulation of Mitochondrial Physiology in Neuroprotection and Neurotoxicity

Submission deadline: 25 May 2024
Special Issue Editor
  • Marcos Roberto de Oliveira, PhD
    Federal University of Rio Grande do Sul Department of Biochemistry Post-Graduate Program in Biological Sciences: Biochemistry Street Ramiro Barcelos, Porto Alegre, Rio Grande do Sul, Brazil; Federal University of Mato Grosso Post-Graduate Program in Chemistry Av. Fernando Correa da Costa, Cuiaba, Mato Grosso, Brazil
    Interests: biochemistry; metabolism; metabolic disorders; neuroprotection; neurotoxicity
Special Issue Information

Dear Colleagues,

Mitochondria are central to the production of adenosine triphosphate (ATP) in nucleated human cells. Moreover, these organelles are a major source of reactive species, mainly due to the presence of the oxidative phosphorylation (OXPHOS) system. The structure and number of mitochondria vary according to the cells’ needs. During human development, mitochondria are required to meet the energetic status of growing cells. Mitochondria also control cell death by apoptosis, which is important for tissues to acquire their mature structure. After completion of the growth phase, mitochondria are still necessary for maintaining cellular health in different ways. Certain stimuli, such as different types of stress, lead to cell adaptation involving mitochondrial responses that are not just limited to the production of ATP. In cells undergoing different types of stress, mitochondrial biogenesis may be required to improve both bioenergetic and redox states. Furthermore, modulation of mitochondrial dynamics (i.e., fusion and fission) may be observed as part of the response to stress, or as a negative consequence resulting from that event. Failure to adapt to stress favors the onset of cellular dysfunction and disease. In neurodegenerative disorders, for example, mitochondrial dysfunction results in bioenergetic collapse, redox impairment, and cell death by various mechanisms. Mitochondrial disorders may also be related to alterations in the function of other organelles, such as peroxisomes and endoplasmic reticulum. This indicates the presence of intricate relationships between different components of human cells during both physiological and pathological conditions. Strategies now exist to prevent and treat mitochondrial disturbances, such as those involving natural or synthetic molecules. Hence, this topic focuses on studies that demonstrate a role for mitochondria in maintaining the health of brain cells, as well as on the effects of modulating mitochondrial physiology on neuroprotection and neurotoxicity. We welcome original research reports, review articles, and perspectives in all areas relating to this topic.

Prof. Dr. Marcos Roberto de Oliveira

Guest Editor

mitochondrial physiology
redox biology
cellular signaling
mitochondrial dysfunction
brain disorders
Manuscript Submission Information

Manuscripts should be submitted via our online editorial system at by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website. Research articles, reviews as well as short communications are preferred. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office to announce on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts will be thoroughly refereed through a double-blind peer-review process. Please visit the Instruction for Authors page before submitting a manuscript. The Article Processing Charge (APC) in this open access journal is 2200 USD. Submitted manuscripts should be well formatted in good English.

Published Paper (1 Paper)
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