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Exclusive Review Papers in Autophagy—Second Edition
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Exclusive Review Papers in Autophagy—Second Edition

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

Deadline for manuscript submissions: 30 June 2025 | Viewed by 9455

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 evolutionarily conserved catabolic process in eukaryotic cells that allows the degradation of superfluous or damaged proteins, protein complexes, and organelles. This mechanism connects the elimination of these otherwise potentially harmful factors with the recycling of macromolecules set free during disposal from 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 the 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 encourage all research groups covering relevant areas within the Section’s scope to submit up-to-date, full-length comprehensive reviews highlighting the latest developments in their field.

Researchers from all over the world are invited to contribute to this Special Issue. Potential contributors and invited authors are requested to provide a tentative title and a short abstract to our Editorial Office (cells@mdpi.com) for pre-evaluation. Please note that papers will still be subject to a thorough and rigorous peer-review process. Following peer review, all papers will be published on an ongoing basis with full open access. 

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

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

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Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (4 papers)

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Review

31 pages, 2545 KiB  
Review
Autophagy and Respiratory Viruses: Mechanisms, Viral Exploitation, and Therapeutic Insights
by Farnaz Aligolighasemabadi, Estera Bakinowska, Kajetan Kiełbowski, Mohammadamin Sadeghdoust, Kevin M. Coombs, Parvaneh Mehrbod and Saeid Ghavami
Cells 2025, 14(6), 418; https://doi.org/10.3390/cells14060418 - 12 Mar 2025
Viewed by 1149
Abstract
Respiratory viruses, such as influenza virus, rhinovirus, coronavirus, and respiratory syncytial virus (RSV), continue to impose a heavy global health burden. Despite existing vaccination programs, these infections remain leading causes of morbidity and mortality, especially among vulnerable populations like children, older adults, and [...] Read more.
Respiratory viruses, such as influenza virus, rhinovirus, coronavirus, and respiratory syncytial virus (RSV), continue to impose a heavy global health burden. Despite existing vaccination programs, these infections remain leading causes of morbidity and mortality, especially among vulnerable populations like children, older adults, and immunocompromised individuals. However, the current therapeutic options for respiratory viral infections are often limited to supportive care, underscoring the need for novel treatment strategies. Autophagy, particularly macroautophagy, has emerged as a fundamental cellular process in the host response to respiratory viral infections. This process not only supports cellular homeostasis by degrading damaged organelles and pathogens but also enables xenophagy, which selectively targets viral particles for degradation and enhances cellular defense. However, viruses have evolved mechanisms to manipulate the autophagy pathways, using them to evade immune detection and promote viral replication. This review examines the dual role of autophagy in viral manipulation and host defense, focusing on the complex interplay between respiratory viruses and autophagy-related pathways. By elucidating these mechanisms, we aim to highlight the therapeutic potential of targeting autophagy to enhance antiviral responses, offering promising directions for the development of effective treatments against respiratory viral infections. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy—Second Edition)
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19 pages, 1759 KiB  
Review
Autophagy and Programmed Cell Death Modalities Interplay in HIV Pathogenesis
by Harpreet Kaur Lamsira, Andrea Sabatini, Serena Ciolfi, Fabiola Ciccosanti, Alessandra Sacchi, Mauro Piacentini and Roberta Nardacci
Cells 2025, 14(5), 351; https://doi.org/10.3390/cells14050351 - 28 Feb 2025
Viewed by 1033
Abstract
Human immunodeficiency virus (HIV) infection continues to be a major global health challenge, affecting 38.4 million according to the Joint United Nations Program on HIV/AIDS (UNAIDS) at the end of 2021 with 1.5 million new infections. New HIV infections increased during the 2 [...] Read more.
Human immunodeficiency virus (HIV) infection continues to be a major global health challenge, affecting 38.4 million according to the Joint United Nations Program on HIV/AIDS (UNAIDS) at the end of 2021 with 1.5 million new infections. New HIV infections increased during the 2 years after the COVID-19 pandemic. Understanding the intricate cellular processes underlying HIV pathogenesis is crucial for developing effective therapeutic strategies. Among these processes, autophagy and programmed cell death modalities, including apoptosis, necroptosis, pyroptosis, and ferroptosis, play pivotal roles in the host–virus interaction dynamics. Autophagy, a highly conserved cellular mechanism, acts as a double-edged sword in HIV infection, influencing viral replication, immune response modulation, and the fate of infected cells. Conversely, apoptosis, a programmed cell death mechanism, is a critical defense mechanism against viral spread and contributes to the depletion of CD4+ T cells, a hallmark of HIV/AIDS progression. This review aims to dissect the complex interplay between autophagy and these programmed cell death modalities in HIV-induced pathogenesis. It highlights the molecular mechanisms involved, their roles in viral persistence and immune dysfunction, and the challenges posed by the viral reservoir and drug resistance, which continue to impede effective management of HIV pathology. Targeting these pathways holds promise for novel therapeutic strategies to mitigate immune depletion and chronic inflammation, ultimately improving outcomes for individuals living with HIV. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy—Second Edition)
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Figure 1

19 pages, 2487 KiB  
Review
Therapeutic Relevance of Inducing Autophagy in β-Thalassemia
by Roberto Gambari and Alessia Finotti
Cells 2024, 13(11), 918; https://doi.org/10.3390/cells13110918 - 25 May 2024
Viewed by 2232
Abstract
The β-thalassemias are inherited genetic disorders affecting the hematopoietic system. In β-thalassemias, more than 350 mutations of the adult β-globin gene cause the low or absent production of adult hemoglobin (HbA). A clinical parameter affecting the physiology of erythroid cells is the excess [...] Read more.
The β-thalassemias are inherited genetic disorders affecting the hematopoietic system. In β-thalassemias, more than 350 mutations of the adult β-globin gene cause the low or absent production of adult hemoglobin (HbA). A clinical parameter affecting the physiology of erythroid cells is the excess of free α-globin. Possible experimental strategies for a reduction in excess free α-globin chains in β-thalassemia are CRISPR-Cas9-based genome editing of the β-globin gene, forcing “de novo” HbA production and fetal hemoglobin (HbF) induction. In addition, a reduction in excess free α-globin chains in β-thalassemia can be achieved by induction of the autophagic process. This process is regulated by the Unc-51-like kinase 1 (Ulk1) gene. The interplay with the PI3K/Akt/TOR pathway, with the activity of the α-globin stabilizing protein (AHSP) and the involvement of microRNAs in autophagy and Ulk1 gene expression, is presented and discussed in the context of identifying novel biomarkers and potential therapeutic targets for β-thalassemia. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy—Second Edition)
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Graphical abstract

34 pages, 1900 KiB  
Review
Molecular Mechanism of Autophagosome–Lysosome Fusion in Mammalian Cells
by Po-Yuan Ke
Cells 2024, 13(6), 500; https://doi.org/10.3390/cells13060500 - 13 Mar 2024
Cited by 9 | Viewed by 4429
Abstract
In eukaryotes, targeting intracellular components for lysosomal degradation by autophagy represents a catabolic process that evolutionarily regulates cellular homeostasis. The successful completion of autophagy initiates the engulfment of cytoplasmic materials within double-membrane autophagosomes and subsequent delivery to autolysosomes for degradation by acidic proteases. [...] Read more.
In eukaryotes, targeting intracellular components for lysosomal degradation by autophagy represents a catabolic process that evolutionarily regulates cellular homeostasis. The successful completion of autophagy initiates the engulfment of cytoplasmic materials within double-membrane autophagosomes and subsequent delivery to autolysosomes for degradation by acidic proteases. The formation of autolysosomes relies on the precise fusion of autophagosomes with lysosomes. In recent decades, numerous studies have provided insights into the molecular regulation of autophagosome–lysosome fusion. In this review, an overview of the molecules that function in the fusion of autophagosomes with lysosomes is provided. Moreover, the molecular mechanism underlying how these functional molecules regulate autophagosome–lysosome fusion is summarized. Full article
(This article belongs to the Special Issue Exclusive Review Papers in Autophagy—Second Edition)
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