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Biomedicines
Special Issues
Mitochondrial Dysfunction and Oxidative Stress
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Mitochondrial Dysfunction and Oxidative Stress

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1040

Special Issue Editor

Dr. Susana Cardoso

E-Mail Website
Guest Editor
Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Interests: diabetes; Alzheimer´s disease; mental disorders; mitochondria; oxidative stress; uncoupling proteins; brain metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria, special double-membrane-bound intracellular organelles found in the cells of most eukaryotes, are universally regarded as the powerhouse of the cell. However, in addition to supplying energy, mitochondria fulfill several other roles that contribute to the regulation of the cell’s proper function, as is the case of reactive oxygen species (ROS) formation and neutralization. Having a recognized role as signaling molecules, ROS, when in excessive levels, elicit an imbalance in cellular redox status, leading to a condition of oxidative stress that can cause damage to organelles, including mitochondria itself, as well as tissues and organs in the body. resulting in a vast number of diseases. As many lines of evidence suggest, perturbations in mitochondria physiological function, energy metabolism regulation and oxidative status are critically linked with the pathophysiology of many neurodevelopmental, neuropsychiatric, and neurodegenerative disorders.

Considering the importance of the subject, this Special Issue intends to collect basic and preclinical studies that may cover all research aspects related to mitochondria homeostasis and deregulation, metabolic disturbances, as well as redox biology and its interplay with diverse brain pathologies that impact the human organism from birth to old age. Comprehensive and critical reviews within the topic are also welcome. 

Dr. Susana Cardoso
Guest Editor

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. Biomedicines 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 2600 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

  • mitochondria
  • oxidative stress
  • brain metabolism
  • neurodevelopmental diseases
  • neuropsychiatric diseases
  • neurodegenerative diseases
  • mitochondrial medicine
  • translational medicine

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Related Special Issue

Published Papers (1 paper)

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Review

30 pages, 1566 KiB  
Review
Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies
by Kai Meng, Haocheng Jia, Xiaoqing Hou, Ziming Zhu, Yuguang Lu, Yingying Feng, Jingwen Feng, Yong Xia, Rubin Tan, Fen Cui and Jinxiang Yuan
Biomedicines 2025, 13(2), 327; https://doi.org/10.3390/biomedicines13020327 - 31 Jan 2025
Viewed by 357
Abstract
Neurodegenerative disease (ND) refers to the progressive loss and morphological abnormalities of neurons in the central nervous system (CNS) or peripheral nervous system (PNS). Examples of neurodegenerative diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Recent studies have [...] Read more.
Neurodegenerative disease (ND) refers to the progressive loss and morphological abnormalities of neurons in the central nervous system (CNS) or peripheral nervous system (PNS). Examples of neurodegenerative diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Recent studies have shown that mitochondria play a broad role in cell signaling, immune response, and metabolic regulation. For example, mitochondrial dysfunction is closely associated with the onset and progression of a variety of diseases, including ND, cardiovascular diseases, diabetes, and cancer. The dysfunction of energy metabolism, imbalance of mitochondrial dynamics, or abnormal mitophagy can lead to the imbalance of mitochondrial homeostasis, which can induce pathological reactions such as oxidative stress, apoptosis, and inflammation, damage the nervous system, and participate in the occurrence and development of degenerative nervous system diseases such as AD, PD, and ALS. In this paper, the latest research progress of this subject is detailed. The mechanisms of oxidative stress, mitochondrial homeostasis, and mitophagy-mediated ND are reviewed from the perspectives of β-amyloid (Aβ) accumulation, dopamine neuron damage, and superoxide dismutase 1 (SOD1) mutation. Based on the mechanism research, new ideas and methods for the treatment and prevention of ND are proposed. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress)
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