Special Issue "Mitochondrial Dysfunction in Ageing and Diseases: Partie Deux"
Deadline for manuscript submissions: 31 July 2021.
Department of Neuroscience, BioMedicum, Karolinska Institutet, Stockholm, Sweden
Interests: mitochondrial dysfunction; metabolism; epigenetics; development; brain plasticity; models for ageing and neurodegenerative diseases and possible treatments
Interests: protein homeostasis, mitochondrial dysfunction; inflammation; models for ageing and age-related diseases and treatment strategies
The past two decades have witnessed an explosion of knowledge regarding how mitochondrial dysfunction may translate into aging and disease phenotypes, as well as how it is modulated by genetic and lifestyle factors. Impairment of the mitochondria may be caused by mutations or deletions in nuclear or mitochondrial DNA as well as by deterioration of quality control mechanisms. Hallmarks of mitochondrial dysfunction include decreased ATP production, decreased mitochondrial membrane potential, swollen mitochondria, damaged cristae, increased oxidative stress, and decreased mitochondrial DNA copy number. In addition to energy production, mitochondria play an important role in regulating apoptosis, buffering calcium release, retrograde signaling to the nuclear genome, producing reactive oxygen species (ROS), participating in steroid synthesis, signaling to the immune system, as well as controlling the cell cycle and cell growth. Dysfunctional mitochondria have been implicated in aging and in numerous diseases, many of which are age-related, including cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, stroke, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease in addition to amyotrophic lateral sclerosis. Additionally, the link between mitochondrial metabolism and the ubiquitin proteasome and autophagy–lysosome systems is continuing to emerge as a novel factor contributing to the progression of aging and several human diseases. Lifestyle factors, such as diet and exercise, as well as small molecules have shown increasing promise as possible treatments to improve energy metabolism. Emerging evidence now also links mitochondrial dysfunction as a key player in innate immunity and chronic inflammation.
Join us as we explore advancements made in the vast field of mitochondrial biology with regards to aging and diseases. This Special Issue serves as an update to a previous issue and calls for original research, mini and full reviews, and perspectives that address the progress and current standing of mitochondrial dysfunction in the following topics:
- dementias and neurodegenerative diseases
- treatments to counteract mitochondrial dysfunction
- protein homeostasis and mtDNA quality control
- chronic inflammation and inflammatory diseases
- cell/retrograde signaling
- oxidative stress
- metabolic disorders and diabetes
Jaime M. Ross, Ph.D.
Giuseppe Coppotelli, Ph.D.
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.
- aging; dementias and neurodegenerative diseases; treatments to counteract mitochondrial dysfunction; protein homeostasis and mtDNA quality control; chronic inflammation and inflammatory diseases; cell/retrograde signaling; oxidative stress; metabolic disorders and diabetes; pain; cancer; stroke
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
1. Proposed title: Hyperhomocysteinemia, thioretinaco ozonide, and mitochondrial dysfunction Short abstract: The discovery of hyperhomocysteinemia as an etiological factor in arteriosclerosis and diseases of aging, including cardiovascular disease, cancer, autoimmune diseases, and neurodegenerative diseases, led to development of the theory of thioretinaco ozonide as the active site of oxidative phosphorylation in mitochondria. Loss of thioretinaco ozonide from mitochondria is promoted by diverse pathogenic, metabolic, nutritional, cellular and molecular factors that predispose to mitochondrial dysfunction in diseases of aging. Therapeutic strategies that prevent loss of thioretinaco ozonide from mitochondria have the potential for treatment and prevention of diseases associated with hyperhomocysteinemia.
2. Role of Redox Signaling in Sarcopenia
Abstract: Sarcopenia is a condition in which skeletal muscle reduces mass and function over age. Severe sarcopenia results in disability, decreased quality of life, and elevated risk of death, and prevails in a growing proportion of the population. The etiological mechanism of sarcopenia is not entirely known. In this review we will focus on the role of reactive oxygen species (ROS) and oxidative stress. Major factors contributing to sarcopenia include mitochondrial dysfunction, impaired autophagy and mitophagy, dysregulation of protein turnover, disruption of AMPK signaling, inflammation, and apoptosis. We propose that change in the sensitivity of redox signaling plays a major role in the development of sarcopenia, whereby various pathways necessary for maintenance of muscle mass and function are differentially affected by ROS and oxidative stress.
3. A mitocentric view of the main bacterial and parasitic infectious diseases in the pediatric population
4. Hyperhomocysteinemia, thioretinaco ozonide, and mitochondrial dysfunction