Oxidative Medicine and Cellular Longevity

Mitochondria at the Crossroads of Survival and Demise


Publishing date
01 Jul 2019
Status
Published
Submission deadline
08 Mar 2019

1University of Duisburg-Essen, Essen, Germany

2University of Padova, Padova, Italy

3The University of Western Australia, Perth, Australia


Mitochondria at the Crossroads of Survival and Demise

Description

Mitochondria are multifunctional organelles and their structural and functional integrity is fundamental to cell life. In addition to their critical role in the production of ATP via oxidative phosphorylation and biosynthetic intermediates, mitochondria are also a major hub for cellular Ca2+ signaling. They decode Ca2+ signals received from the endoplasmic reticulum into specific inputs to regulate essential functions including metabolism and energy production. However, mitochondria can actively or passively drive cellular dysfunction or demise. They can become the major source of reactive oxygen species in pathological processes and reversely they are highly vulnerable to damage. Thereby, mitochondria represent a point of convergence for a variety of upstream cell death stimuli and undergo structural and functional remodeling with subsequent transmission of signals to downstream executioner proteins. The intrinsic pathway includes death stimuli like lack of dioxygen, metabolic perturbation, deprivation of survival factors, oxidative stress, Ca2+ overload, DNA damage, proteotoxic stress, and oncogene activation. In response to this diversity of stimuli mitochondria are central to several different modes of regulated cell death like apoptosis and necrosis. Initial events in mitochondria leading to apoptosis are the permeability transition in the inner membrane leading to outer membrane rupture and the permeabilization of the outer membrane permitting the release of apoptogenic factors from the mitochondrial intermembrane space. Necrosis is characterized by mitochondrial membrane depolarization, decreased ATP levels, cellular and organellar swelling, and loss of plasma membrane integrity. These signaling pathways are highly orchestrated as well as integrated at the molecular level and overlap substantially with respect to disease. Based on their pathophysiological importance, mitochondria have attracted broad scientific and clinical interest as an important target for intervention in disease.

We invite investigators to contribute original research articles as well as review articles that will advance our understanding of the mitochondria behavior and function in response to oxidative stress in disease/disorders such as cardiovascular and neurodegenerative diseases, which could be important for the development of new mechanism-based pharmacotherapeutic strategies to treat many human diseases.

Potential topics include but are not limited to the following:

  • Regulation of mitochondrial energy production in health and disease progression
  • Involvement of mitochondrial perturbation in regulated cell death
  • Mitochondrial outer and inner membrane permeabilization: structure and assembly of the pores
  • Calcium overload and mitochondrial damage
  • Endoplasmic reticulum-mitochondria tethering: the role of MAMs (mitochondria-associated membranes) in health and disease progression
  • Physical composition of mitochondria and their physical location within the cell in health and disease progression
  • Role of mitochondrial reverse electron transport in ROS signaling in health and disease progression

Articles

  • Special Issue
  • - Volume 2019
  • - Article ID 2608187
  • - Editorial

Mitochondria at the Crossroads of Survival and Demise

Ulrike B. Hendgen-Cotta | Valentina Giorgio | Livia Hool
  • Special Issue
  • - Volume 2019
  • - Article ID 1681254
  • - Research Article

Overexpression of Mitochondrial Calcium Uniporter Causes Neuronal Death

Veronica Granatiero | Marco Pacifici | ... | Rosario Rizzuto
  • Special Issue
  • - Volume 2019
  • - Article ID 1845321
  • - Research Article

Crosstalk between Mitochondrial Ca2+ Uptake and Autophagy in Skeletal Muscle

Gaia Gherardi | Giulia Di Marco | ... | Cristina Mammucari
  • Special Issue
  • - Volume 2019
  • - Article ID 3904905
  • - Research Article

Vanillic Acid Restores Coenzyme Q Biosynthesis and ATP Production in Human Cells Lacking COQ6

Manuel J. Acosta Lopez | Eva Trevisson | ... | Leonardo Salviati
  • Special Issue
  • - Volume 2019
  • - Article ID 7683051
  • - Research Article

Nanoencapsulated Quercetin Improves Cardioprotection during Hypoxia-Reoxygenation Injury through Preservation of Mitochondrial Function

Omar Lozano | Anay Lázaro-Alfaro | ... | Gerardo García-Rivas
  • Special Issue
  • - Volume 2019
  • - Article ID 7058350
  • - Review Article

Stay Fit, Stay Young: Mitochondria in Movement: The Role of Exercise in the New Mitochondrial Paradigm

Jesus R. Huertas | Rafael A. Casuso | ... | Sara Cogliati
  • Special Issue
  • - Volume 2019
  • - Article ID 7210892
  • - Review Article

Mitochondrial Dysfunctions: A Thread Sewing Together Alzheimer’s Disease, Diabetes, and Obesity

Giulia Rigotto | Emy Basso
  • Special Issue
  • - Volume 2019
  • - Article ID 7976382
  • - Research Article

High Concentration of Low-Density Lipoprotein Results in Disturbances in Mitochondrial Transcription and Functionality in Endothelial Cells

Stefanie Gonnissen | Johannes Ptok | ... | Joachim Altschmied
  • Special Issue
  • - Volume 2019
  • - Article ID 7210249
  • - Research Article

Fetal Programming and Sexual Dimorphism of Mitochondrial Protein Expression and Activity of Hearts of Prenatally Hypoxic Guinea Pig Offspring

Loren P. Thompson | Hong Song | Brian M. Polster
  • Special Issue
  • - Volume 2019
  • - Article ID 9537504
  • - Research Article

Mitochondrial Transfer of Wharton’s Jelly Mesenchymal Stem Cells Eliminates Mutation Burden and Rescues Mitochondrial Bioenergetics in Rotenone-Stressed MELAS Fibroblasts

Tsu-Kung Lin | Shang-Der Chen | ... | Chia-Wei Liou
Oxidative Medicine and Cellular Longevity
 Journal metrics
Acceptance rate49%
Submission to final decision75 days
Acceptance to publication38 days
CiteScore4.520
Impact Factor4.868
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