Oxidative Medicine and Cellular Longevity

Transautophagy: Research and Translation of Autophagy Knowledge


Status
Published

1University of Urbino “Carlo Bo”, Urbino, Italy

2Eberhard Karls University of Tuebingen, Tuebingen, Germany

3University of Oslo, Oslo, Norway

4Institut Jozef Stefan, Ljubljana, Slovenia

5University of Bristol, Bristol, UK


Transautophagy: Research and Translation of Autophagy Knowledge

Description

Autophagy is an essential mechanism to sustain homeostasis at cellular and organismal levels. Concerning human health, an increasing number of examples underline its value as a novel therapeutic target since autophagy modulation may potentially become an effective new strategy to combat cancer, neurodegeneration, and infection. Beneficially, autophagy modulation may also slow down age-related tissue decline. A relationship between redox disorder and autophagy signaling has already been described but is still not well characterized. Oxidative stress can arise in cells because of different reasons; among them are metal imbalance and perturbation or perforation of cellular membranes by various insults. In addition, it has been recently hypothesized that amyloid prefibrillar oligomers and proteostasis constitute a metabolic balance between synthesis and degradation of proteins, with protein misfolding and accumulation of the aggregated proteins shifting the balance. All these processes are in direct or indirect way relying on good performance of autophagy to clear the cells of unnecessary burdens and thus rejuvenate them.

In the recognition of the intense increase of autophagy research in health and disease European network called Transautophagy (COST Action CA15138) has been created to promote multidisciplinary research on autophagy and to exploit this knowledge for biomedical and biotechnological purposes. The spectrum of expected outcomes ranges from recommendations for healthy aging or disease prevention to the discovery of new therapies, bio-based components, or nanodevices capable of selectively modulating autophagy.

This special issue aims to collect high quality papers interesting to the broader audience of this journal. We are inviting authors to contribute high quality research articles and reviews.

Potential topics include but are not limited to the following:

  • Crosstalk between ROS and autophagy signaling
  • Autophagy as a regulatory mechanism of protein aggregation and oxidative stress
  • Role of metals-to-protein aggregation in oxidative stress associated autophagy
  • Mechanism of action of antioxidant substances on autophagy modulation
  • Lipid composition of membranes and interaction of lipid rafts with misfolded species
  • Sensors of protein aggregation and oxidative stress in a cell and main signaling pathways
  • Overview about possible autophagy based approaches to promote healthy aging
  • Compendium procedures for stage specific assessment of autophagy activity
  • Basic knowledge on autophagy to improve molecular understanding of the main mechanisms that regulate autophagy pathways
  • Autophagy analyses and modulation
  • Functions and dysfunctions of autophagy in cellular and animal models of human diseases with the ultimate objective of providing the basis for the development of novel biomedical applications
  • Review of collecting data derived from the analysis of autophagy modulation in preclinical models of disease
  • Translation of research results into benefits to patients by tackling i) biomarker discovery, ii) development of strategies to foster healthy aging, and iii) development of therapeutic strategies to treat a variety of diseases

Articles

  • Special Issue
  • - Volume 2018
  • - Article ID 7504165
  • - Editorial

Transautophagy: Research and Translation of Autophagy Knowledge

Maria C. Albertini | Tassula Proikas-Cezanne | ... | Jon D. Lane
  • Special Issue
  • - Volume 2018
  • - Article ID 4043726
  • - Research Article

SGK1 Inhibits Autophagy in Murine Muscle Tissue

Theresia Zuleger | Julia Heinzelbecker | ... | Tassula Proikas-Cezanne
  • Special Issue
  • - Volume 2018
  • - Article ID 4968321
  • - Research Article

From Oxidative Stress Damage to Pathways, Networks, and Autophagy via MicroRNAs

Nikolai Engedal | Eva Žerovnik | ... | Maria Cristina Albertini
  • Special Issue
  • - Volume 2018
  • - Article ID 8067592
  • - Research Article

Oleuropein Aglycone Protects against MAO-A-Induced Autophagy Impairment and Cardiomyocyte Death through Activation of TFEB

Caterina Miceli | Yohan Santin | ... | Chiara Nediani
  • Special Issue
  • - Volume 2018
  • - Article ID 8613209
  • - Research Article

Inhibition of Protein Aggregation by Several Antioxidants

Samra Hasanbašić | Alma Jahić | ... | Eva Žerovnik
  • Special Issue
  • - Volume 2018
  • - Article ID 1482795
  • - Research Article

Low Autophagy (ATG) Gene Expression Is Associated with an Immature AML Blast Cell Phenotype and Can Be Restored during AML Differentiation Therapy

Jing Jin | Adrian Britschgi | ... | Mario P. Tschan
  • Special Issue
  • - Volume 2018
  • - Article ID 2450748
  • - Review Article

The Role of Free Radicals in Autophagy Regulation: Implications for Ageing

M. Pajares | A. Cuadrado | ... | M. Cahova
  • Special Issue
  • - Volume 2018
  • - Article ID 8023821
  • - Review Article

Autophagy Modulation in Cancer: Current Knowledge on Action and Therapy

Mija Marinković | Matilda Šprung | ... | Ivana Novak
  • Special Issue
  • - Volume 2018
  • - Article ID 6721530
  • - Research Article

Epigallocatechin-3-Gallate (EGCG) Promotes Autophagy-Dependent Survival via Influencing the Balance of mTOR-AMPK Pathways upon Endoplasmic Reticulum Stress

Marianna Holczer | Boglárka Besze | ... | Orsolya Kapuy
  • Special Issue
  • - Volume 2017
  • - Article ID 7120962
  • - Review Article

The Crosstalk between ROS and Autophagy in the Field of Transplantation Medicine

Anne C. Van Erp | Dane Hoeksma | ... | Jean-Paul Decuypere
Oxidative Medicine and Cellular Longevity
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Acceptance rate8%
Submission to final decision133 days
Acceptance to publication34 days
CiteScore10.100
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