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Exclusive Review Papers in Autophagy
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Exclusive Review Papers in Autophagy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (15 September 2023) | Viewed by 15541

Special Issue Editor

Dr. Harald W. Platta

E-Mail Website
Guest Editor
Biochemie Intrazellulärer Transportprozesse, Institut für Biochemie & Pathobiochemie, Ruhr-Universität, Bochum, Germany
Interests: ubiquitin; autophagy; protein targeting; peroxisomes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is an evolutionary conserved catabolic process in eukaryotic cells which allows the degradation of superfluous or damaged proteins, protein complexes, and organelles. This mechanism connects the elimination of these otherwise potential harmful factors with the recycling of macromolecules set free during the disposal within lysosomes or vacuoles. This clearance, which can be induced or constitutive, is a protective mechanism against cellular stress as well as invading pathogens. As a result, distinct autophagy pathways are involved in a multitude of physiological functions and pathological situations.

Autophagy is currently one of the fastest-growing research areas in life and medical sciences. Under the section “Autophagy”, this Special Issue aims to present high-quality review articles detailing the latest cutting-edge research on autophagy in different species. We kindly encourage all research groups covering relevant areas within the section’s scope to contribute up-to-date, full-length comprehensive reviews, highlighting the latest developments in their research field.

Distinguished researchers from all over the world will be invited to contribute to this Special Issue. Potential contributors/invited authors are kindly requested to submit a tentative title and a short abstract to our Editorial Office ([email protected]) for pre-evaluation. Please note that selected full papers will still be subject to a thorough and rigorous peer review. All papers will be published on an ongoing basis. Papers will be published with full open access after peer review.

Dr. Harald W. Platta
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • ubiquitination
  • autophagy
  • peroxisomes
  • macroautophagy
  • pexophagy
  • mitophagy
  • lysosome
  • vacuole
  • organellar homeostasis
  • posttranslational modifications
  • lipids
  • signaling cascades

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Related Special Issue

Published Papers (5 papers)

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Research

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21 pages, 27931 KiB  
Article
Loss of Pex1 in Inner Ear Hair Cells Contributes to Cochlear Synaptopathy and Hearing Loss
by Stephanie A. Mauriac, Thibault Peineau, Aamir Zuberi, Cathleen Lutz and Gwénaëlle S. G. Géléoc
Cells 2022, 11(24), 3982; https://doi.org/10.3390/cells11243982 - 9 Dec 2022
Viewed by 2706
Abstract
Peroxisome Biogenesis Disorders (PBD) and Zellweger syndrome spectrum disorders (ZSD) are rare genetic multisystem disorders that include hearing impairment and are associated with defects in peroxisome assembly, function, or both. Mutations in 13 peroxin (PEX) genes have been found to cause [...] Read more.
Peroxisome Biogenesis Disorders (PBD) and Zellweger syndrome spectrum disorders (ZSD) are rare genetic multisystem disorders that include hearing impairment and are associated with defects in peroxisome assembly, function, or both. Mutations in 13 peroxin (PEX) genes have been found to cause PBD-ZSD with ~70% of patients harboring mutations in PEX1. Limited research has focused on the impact of peroxisomal disorders on auditory function. As sensory hair cells are particularly vulnerable to metabolic changes, we hypothesize that mutations in PEX1 lead to oxidative stress affecting hair cells of the inner ear, subsequently resulting in hair cell degeneration and hearing loss. Global deletion of the Pex1 gene is neonatal lethal in mice, impairing any postnatal studies. To overcome this limitation, we created conditional knockout mice (cKO) using Gfi1Creor VGlut3Cre expressing mice crossed to floxed Pex1 mice to allow for selective deletion of Pex1 in the hair cells of the inner ear. We find that Pex1 excision in inner hair cells (IHCs) leads to progressive hearing loss associated with significant decrease in auditory brainstem responses (ABR), specifically ABR wave I amplitude, indicative of synaptic defects. Analysis of IHC synapses in cKO mice reveals a decrease in ribbon synapse volume and functional alterations in exocytosis. Concomitantly, we observe a decrease in peroxisomal number, indicative of oxidative stress imbalance. Taken together, these results suggest a critical function of Pex1 in development and maturation of IHC-spiral ganglion synapses and auditory function. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy)
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Review

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17 pages, 2712 KiB  
Review
Update on Autophagy Inhibitors in Cancer: Opening up to a Therapeutic Combination with Immune Checkpoint Inhibitors
by Eloïne Bestion, Eric Raymond, Soraya Mezouar and Philippe Halfon
Cells 2023, 12(13), 1702; https://doi.org/10.3390/cells12131702 - 23 Jun 2023
Cited by 6 | Viewed by 2719
Abstract
Autophagy is a highly conserved and natural degradation process that helps maintain cell homeostasis through the elimination of old, worn, and defective cellular components, ensuring proper cell energy intake. The degradative pathway constitutes a protective barrier against diverse human diseases including cancer. Autophagy [...] Read more.
Autophagy is a highly conserved and natural degradation process that helps maintain cell homeostasis through the elimination of old, worn, and defective cellular components, ensuring proper cell energy intake. The degradative pathway constitutes a protective barrier against diverse human diseases including cancer. Autophagy basal level has been reported to be completely dysregulated during the entire oncogenic process. Autophagy influences not only cancer initiation, development, and maintenance but also regulates cancer response to therapy. Currently, autophagy inhibitor candidates mainly target the early autophagy process without any successful preclinical/clinical development. Lessons learned from autophagy pharmaceutical manipulation as a curative option progressively help to improve drug design and to encounter new targets of interest. Combinatorial strategies with autophagy modulators are supported by abundant evidence, especially dealing with immune checkpoint inhibitors, for which encouraging preclinical results have been recently published. GNS561, a PPT1 inhibitor, is a promising autophagy modulator as it has started a phase 2 clinical trial in liver cancer indication, combined with atezolizumab and bevacizumab, an assessment without precedent in the field. This approach paves a new road, leading to the resurgence of anticancer autophagy inhibitors as an attractive therapeutic target in cancer. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy)
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15 pages, 1593 KiB  
Review
Autophagosome Biogenesis
by Yan Zhen and Harald Stenmark
Cells 2023, 12(4), 668; https://doi.org/10.3390/cells12040668 - 20 Feb 2023
Cited by 16 | Viewed by 4243
Abstract
Autophagy–the lysosomal degradation of cytoplasm–plays a central role in cellular homeostasis and protects cells from potentially harmful agents that may accumulate in the cytoplasm, including pathogens, protein aggregates, and dysfunctional organelles. This process is initiated by the formation of a phagophore membrane, which [...] Read more.
Autophagy–the lysosomal degradation of cytoplasm–plays a central role in cellular homeostasis and protects cells from potentially harmful agents that may accumulate in the cytoplasm, including pathogens, protein aggregates, and dysfunctional organelles. This process is initiated by the formation of a phagophore membrane, which wraps around a portion of cytoplasm or cargo and closes to form a double-membrane autophagosome. Upon the fusion of the autophagosome with a lysosome, the sequestered material is degraded by lysosomal hydrolases in the resulting autolysosome. Several alternative membrane sources of autophagosomes have been proposed, including the plasma membrane, endosomes, mitochondria, endoplasmic reticulum, lipid droplets, hybrid organelles, and de novo synthesis. Here, we review recent progress in our understanding of how the autophagosome is formed and highlight the proposed role of vesicles that contain the lipid scramblase ATG9 as potential seeds for phagophore biogenesis. We also discuss how the phagophore is sealed by the action of the endosomal sorting complex required for transport (ESCRT) proteins. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy)
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18 pages, 1837 KiB  
Review
A Review on Autophagy in Orofacial Neuropathic Pain
by Mayank Shrivastava and Liang Ye
Cells 2022, 11(23), 3842; https://doi.org/10.3390/cells11233842 - 30 Nov 2022
Cited by 4 | Viewed by 2334
Abstract
Orofacial neuropathic pain indicates pain caused by a lesion or diseases of the somatosensory nervous system. It is challenging for the clinician to diagnose and manage orofacial neuropathic pain conditions due to the considerable variability between individual clinical presentations and a lack of [...] Read more.
Orofacial neuropathic pain indicates pain caused by a lesion or diseases of the somatosensory nervous system. It is challenging for the clinician to diagnose and manage orofacial neuropathic pain conditions due to the considerable variability between individual clinical presentations and a lack of understanding of the mechanisms underlying the etiology and pathogenesis. In the last few decades, researchers have developed diagnostic criteria, questionnaires, and clinical assessment methods for the diagnosis of orofacial neuropathic pain. Recently, researchers have observed the role of autophagy in neuronal dysfunction as well as in the modulation of neuropathic pain. On this basis, in the present review, we highlight the characteristics, classification, and clinical assessment of orofacial neuropathic pain. Additionally, we introduce autophagy and its potential role in the modulation of orofacial neuropathic pain, along with a brief overview of the pathogenesis, which in future may reveal new possible targets for treating this condition. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy)
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15 pages, 724 KiB  
Review
The Role of the miR-17-92 Cluster in Autophagy and Atherosclerosis Supports Its Link to Lysosomal Storage Diseases
by Daniel Ortuño-Sahagún, Julia Enterría-Rosales, Vanesa Izquierdo, Christian Griñán-Ferré, Mercè Pallàs and Celia González-Castillo
Cells 2022, 11(19), 2991; https://doi.org/10.3390/cells11192991 - 26 Sep 2022
Cited by 2 | Viewed by 2409
Abstract
Establishing the role of non-coding RNA (ncRNA), especially microRNAs (miRNAs), in the regulation of cell function constitutes a current research challenge. Two to six miRNAs can act in clusters; particularly, the miR-17-92 family, composed of miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a is [...] Read more.
Establishing the role of non-coding RNA (ncRNA), especially microRNAs (miRNAs), in the regulation of cell function constitutes a current research challenge. Two to six miRNAs can act in clusters; particularly, the miR-17-92 family, composed of miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a is well-characterized. This cluster functions during embryonic development in cell differentiation, growth, development, and morphogenesis and is an established oncogenic cluster. However, its role in the regulation of cellular metabolism, mainly in lipid metabolism and autophagy, has received less attention. Here, we argue that the miR-17-92 cluster is highly relevant for these two processes, and thus, could be involved in the study of pathologies derived from lysosomal deficiencies. Lysosomes are related to both processes, as they control cholesterol flux and regulate autophagy. Accordingly, we compiled, analyzed, and discussed current evidence that highlights the cluster’s fundamental role in regulating cellular energetic metabolism (mainly lipid and cholesterol flux) and atherosclerosis, as well as its critical participation in autophagy regulation. Because these processes are closely related to lysosomes, we also provide experimental data from the literature to support our proposal that the miR-17-92 cluster could be involved in the pathogenesis and effects of lysosomal storage diseases (LSD). Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy)
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