Special Issue "Autophagy in Age-Related Human Diseases"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling and Regulated Cell Death".

Deadline for manuscript submissions: 31 December 2018

Special Issue Editor

Guest Editor
Prof. Dr. Tassula Proikas-Cezanne

Department of Molecular Biology, Interfaculty Institute of Cell Biology, Eberhard Karls University Tuebingen, Tuebingen, Germany
Website | E-Mail
Phone: +49 7071 29-78895
Fax: +49 7071 29-5359
Interests: autophagy; longevity; tumor metabolism; WIPI genes

Special Issue Information

Dear Colleagues,

Increasingly, the process of autophagy (“self-eating”) is attracting tremendous research efforts. Exciting new data are shedding light on the molecular details of the process of autophagy and its pertubation in human diseases. Moreover, it is becoming evident that autophagy activity and capacity decrease during the aging process, giving rise to the onset of a great variety of age-related diseases. Strikingly, autophagy is also essential to the development of certain diseases (e.g. tumor progression). Hence, the modulation of autophagy is regarded as a new therapeutic opportunity for the future treatment of many pathological conditions. Further, targeting autophagy during the aging process may in fact prove to effectively prevent the onset of age-related human diseases. However, specific autophagy modulators have not yet been developed and tested.

This special issue aims to summarize the current knowledge on the role of autophagy in the process of aging and in age-related human diseases such as neurodegeneration and cancer.

We look forward to your contributions.

Prof. Dr. Tassula Proikas-Cezanne
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 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. Cells 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 1000 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

  • autophagy
  • aging
  • longevity
  • cancer
  • neurodegeneration

Published Papers (3 papers)

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Research

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Open AccessArticle The Precision Control of Autophagic Flux and Vesicle Dynamics—A Micropattern Approach
Received: 3 July 2018 / Revised: 31 July 2018 / Accepted: 31 July 2018 / Published: 3 August 2018
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Abstract
Autophagy failure is implicated in age-related human disease. A decrease in the rate of protein degradation through the entire autophagy pathway, i.e., autophagic flux, has been associated with the onset of cellular proteotoxity and cell death. Although the precision control of autophagy as
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Autophagy failure is implicated in age-related human disease. A decrease in the rate of protein degradation through the entire autophagy pathway, i.e., autophagic flux, has been associated with the onset of cellular proteotoxity and cell death. Although the precision control of autophagy as a pharmacological intervention has received major attention, mammalian model systems that enable a dissection of the relationship between autophagic flux and pathway intermediate pool sizes remain largely underexplored. Here, we make use of a micropattern-based fluorescence life cell imaging approach, allowing a high degree of experimental control and cellular geometry constraints. By assessing two autophagy modulators in a system that achieves a similarly raised autophagic flux, we measure their impact on the pathway intermediate pool size, autophagosome velocity, and motion. Our results reveal a differential effect of autophagic flux enhancement on pathway intermediate pool sizes, velocities, and directionality of autophagosome motion, suggesting distinct control over autophagy function. These findings may be of importance for better understanding the fine-tuning autophagic activity and protein degradation proficiency in different cell and tissue types of age-associated pathologies. Full article
(This article belongs to the Special Issue Autophagy in Age-Related Human Diseases)
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Open AccessArticle Novel Modulators of Proteostasis: RNAi Screen of Chromosome I in a Heat Stress Paradigm in C. elegans
Received: 26 March 2018 / Revised: 17 May 2018 / Accepted: 24 May 2018 / Published: 26 May 2018
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Abstract
Proteostasis is of vital importance for cellular function and it is challenged upon exposure to acute or chronic insults during neurodegeneration and aging. The proteostasis network is relevant for the maintenance of proteome integrity and mainly comprises molecular chaperones and two degradation pathways,
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Proteostasis is of vital importance for cellular function and it is challenged upon exposure to acute or chronic insults during neurodegeneration and aging. The proteostasis network is relevant for the maintenance of proteome integrity and mainly comprises molecular chaperones and two degradation pathways, namely, autophagy and the ubiquitin proteasome system. This network is characterized by an impressive functional interrelation and complexity, and occasionally novel factors are discovered that modulate proteostasis. Here, we present an RNAi screen in C. elegans, which aimed to identify modulators of proteostasis in a heat stress paradigm. The screen comprised genes that are located on chromosome I of the nematode and has identified 185 genetic modifiers, whose knockdown has enhanced the misfolding of a reporter protein upon temperature increase. Subsequently, we evaluated the effect of a distinct number of the identified candidates in an additional C. elegans model strain, which expresses the aggregation-prone PolyQ35::YFP protein. Moreover, we annotated the human orthologs of the identified proteins and analyzed their enrichment in functional clusters and, as appropriate, their association with human neuropathologies. The achieved data collection includes several factors that have already been functionally associated with the proteostasis network, which highlights the potential of this heat stress-based proteostasis screen in order to detect novel modulators of proteome integrity. Full article
(This article belongs to the Special Issue Autophagy in Age-Related Human Diseases)
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Review

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Open AccessFeature PaperReview Autophagy in Age-Associated Neurodegeneration
Received: 2 April 2018 / Revised: 23 April 2018 / Accepted: 3 May 2018 / Published: 5 May 2018
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Abstract
The elimination of abnormal and dysfunctional cellular constituents is an essential prerequisite for nerve cells to maintain their homeostasis and proper function. This is mainly achieved through autophagy, a process that eliminates abnormal and dysfunctional cellular components, including misfolded proteins and damaged organelles.
[...] Read more.
The elimination of abnormal and dysfunctional cellular constituents is an essential prerequisite for nerve cells to maintain their homeostasis and proper function. This is mainly achieved through autophagy, a process that eliminates abnormal and dysfunctional cellular components, including misfolded proteins and damaged organelles. Several studies suggest that age-related decline of autophagy impedes neuronal homeostasis and, subsequently, leads to the progression of neurodegenerative disorders due to the accumulation of toxic protein aggregates in neurons. Here, we discuss the involvement of autophagy perturbation in neurodegeneration and present evidence indicating that upregulation of autophagy holds potential for the development of therapeutic interventions towards confronting neurodegenerative diseases in humans. Full article
(This article belongs to the Special Issue Autophagy in Age-Related Human Diseases)
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Planned Papers

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. Tentative title: Infections in aging: a link between autophagy and senesce
Author: Dr. Maria Isabel Colombo
Affiliation: Consejo Nacional de Investigaciones Cientificas y Tecnicas, Buenos Aires, Argentina

2. Tentative title: Autophagy in age-associated neurodegeneration
Author: Prof. Nektarios Tavernarakis
Affiliation: Foundation for Research and Technology-Hellas, Institute of Molecular Biology and Biotechnology, Heraklion, Greece

3. Tentative title: Autophagy in brain functions
Author: Dr. Patrice Codogno
Affiliation: CNRS Centre National de la Recherche Scientifique, Paris, France

4. Tentative title: Autophagy in metabolic age-related human diseases
Authors: James T. Murray and Cecile Vindis
Abstract: Autophagy is a highly conserved mechanism that mediates degradation of unhealthy organelles, protein aggregates, and invading pathogens, as well as recycling of cellular components that ultimately contributes to cellular renovation and homeostasis maintenance. In the last few years specific functions for autophagy have been identified in many tissues and organs. However dysregulation of autophagy has been identified as a feature of various pathologic states. Here, we review the current knowledge on the role of autophagy, from its regulation to its physiological influence, on metabolic age-related disorders. Finally, we will discuss the therapeutic potential of pharmacological and nutritional modulators of autophagy for treatment of metabolic diseases.

5. Tentative title: Novel modulators of proteostasis in C. elegans: RNAi screen of chromosome I in a heat stress paradigm
Authors: Andreas Kern, Natalie Spang, Heike Huesmann, Christian Behl
Affiliation: Johannes Gutenberg Universitat Mainz, Institute of Physiological Chemistry and Pathobiochemistry, Mainz, Germany

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