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The Role of Autophagy in Disease and Cancer
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The Role of Autophagy in Disease and Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 April 2025) | Viewed by 4740

Special Issue Editors

Dr. Antonio Ieni

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Guest Editor
Department of Human Pathology "Gaetano Barresi", Section of Anatomic Pathology, University of Messina, 98123 Messina, Italy
Interests: autophagy; molecular biology; pathology; epidermal growth factor receptors family; cancer
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Giovanni Tuccari

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Guest Editor
Dipartimento di Patologia Umana Dell’adulto e Dell’età Evolutiva Gaetano Barresi, Divisione di Anatomia Patologica, Università Degli Studi di Messina, 98125 Messina, Italy
Interests: autophagy; molecular biology; pathology; innate immunity; gastritis; Helicobacter pylori; neutrophils; mast cell
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is an important intracellular degradation mechanism that occurs due to various stressful conditions, including the accumulation of damaged proteins and organelles, as well as nutrient deficiency. Previous studies have suggested that mutations in autophagy-related processes could be implicated in human diseases, including infections, cancer, aging, neurodegeneration and metabolic diseases. Comprehensive research is currently being performed in order to discover novel therapeutic markers that are able to modulate the autophagic process in vivo. This evidence has shown that a large number of bioactive drugs are involved in the regulation of autophagy via the modulation of several transcriptional factors and signaling pathways. On the other hand, the most important critical issue is represented by the limited availability of therapeutic drugs and the lack of clinical trials. In this context, the need for an adequate understanding of the complex role of autophagy in human pathologies should be clearly highlighted; this is in order to promote the discovery of new potential targets to enhance the outcome of therapeutic strategy.

This Special Issue will focus on the mechanism of autophagy in human disease for therapeutic purposes. We are pleased to invite authors to submit original articles that provide novel findings or reviews that comprehensively highlight the latest discoveries in the field.

I look forward to receiving your contributions.

Dr. Antonio Ieni
Prof. Dr. Giovanni Tuccari
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • autophagy-related proteins
  • target therapy
  • cancer
  • neurodegenerative disease
  • infections
  • aging
  • metabolic disease
  • autoimmunity

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Published Papers (3 papers)

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Research

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10 pages, 1919 KiB  
Article
Role of ATG4 Autophagy-Related Protein Family in the Lower Airways of Patients with Stable COPD
by Francesco Nucera, Antonino Di Stefano, Fabio Luigi Massimo Ricciardolo, Isabella Gnemmi, Cristina Pizzimenti, Francesco Monaco, Giovanni Tuccari, Gaetano Caramori and Antonio Ieni
Int. J. Mol. Sci. 2024, 25(15), 8182; https://doi.org/10.3390/ijms25158182 - 26 Jul 2024
Cited by 1 | Viewed by 1376
Abstract
Autophagy is a complex physiological pathway mediating homeostasis and survival of cells degrading damaged organelles and regulating their recycling. Physiologic autophagy can maintain normal lung function, decrease lung cellular senescence, and inhibit myofibroblast differentiation. It is well known that autophagy is activated in [...] Read more.
Autophagy is a complex physiological pathway mediating homeostasis and survival of cells degrading damaged organelles and regulating their recycling. Physiologic autophagy can maintain normal lung function, decrease lung cellular senescence, and inhibit myofibroblast differentiation. It is well known that autophagy is activated in several chronic inflammatory diseases; however, its role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and the expression of autophagy-related genes (ATGs) in lower airways of COPD patients is still controversial. The expression and localization of all ATG proteins that represented key components of the autophagic machinery modulating elongation, closure, and maturation of autophagosome membranes were retrospectively measured in peripheral lungs of patients with stable COPD (n = 10), control smokers with normal lung function (n = 10), and control nonsmoking subjects (n = 8) using immunohistochemical analysis. These results show an increased expression of ATG4 protein in alveolar septa and bronchiolar epithelium of stable COPD patients compared to smokers with normal lung function and non-smoker subjects. In particular, the genes in the ATG4 protein family (including ATG4A, ATG4B, ATG4C, and ATG4D) that have a key role in the modulation of the physiological autophagic machinery are the most important ATGs increased in the compartment of lower airways of stable COPD patients, suggesting that the alteration shown in COPD patients can be also correlated to impaired modulation of autophagic machinery modulating elongation, closure, and maturation of autophagosomes membranes. Statistical analysis was performed by the Kruskal–Wallis test and the Mann–Whitney U test for comparison between groups. A statistically significant increased expression of ATG4A (p = 0.0047), ATG4D (p = 0.018), and ATG5 (p = 0.019) was documented in the bronchiolar epithelium as well in alveolar lining for ATG4A (p = 0.0036), ATG4B (p = 0.0054), ATG4C (p = 0.0064), ATG4D (p = 0.0084), ATG5 (p = 0.0088), and ATG7 (p = 0.018) in patients with stable COPD compared to control groups. The ATG4 isoforms may be considered as additional potential targets for the development of new drugs in COPD. Full article
(This article belongs to the Special Issue The Role of Autophagy in Disease and Cancer)
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Review

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20 pages, 1427 KiB  
Review
Current Understanding of the Role of Autophagy in the Treatment of Myeloid Leukemia
by Yasushi Kubota and Shinya Kimura
Int. J. Mol. Sci. 2024, 25(22), 12219; https://doi.org/10.3390/ijms252212219 - 14 Nov 2024
Viewed by 1392
Abstract
The most important issues in acute myeloid leukemia are preventing relapse and treating relapse. Although the remission rate has improved to approximately 80%, the 5-year survival rate is only around 30%. The main reasons for this are the high relapse rate and the [...] Read more.
The most important issues in acute myeloid leukemia are preventing relapse and treating relapse. Although the remission rate has improved to approximately 80%, the 5-year survival rate is only around 30%. The main reasons for this are the high relapse rate and the limited treatment options. In chronic myeloid leukemia patients, when a deep molecular response is achieved for a certain period of time through tyrosine kinase inhibitor treatment, about half of them will reach treatment-free remission, but relapse is still a problem. Therefore, potential therapeutic targets for myeloid leukemias are eagerly awaited. Autophagy suppresses the development of cancer by maintaining cellular homeostasis; however, it also promotes cancer progression by helping cancer cells survive under various metabolic stresses. In addition, autophagy is promoted or suppressed in cancer cells by various genetic mutations. Therefore, the development of therapies that target autophagy is also being actively researched in the field of leukemia. In this review, studies of the role of autophagy in hematopoiesis, leukemogenesis, and myeloid leukemias are presented, and the impact of autophagy regulation on leukemia treatment and the clinical trials of autophagy-related drugs to date is discussed. Full article
(This article belongs to the Special Issue The Role of Autophagy in Disease and Cancer)
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16 pages, 1288 KiB  
Review
Autophagy as a Guardian of Vascular Niche Homeostasis
by Konstantin Dergilev, Alexandre Gureenkov and Yelena Parfyonova
Int. J. Mol. Sci. 2024, 25(18), 10097; https://doi.org/10.3390/ijms251810097 - 20 Sep 2024
Cited by 2 | Viewed by 1214
Abstract
The increasing burden of vascular dysfunction on healthcare systems worldwide results in higher morbidity and mortality rates across pathologies, including cardiovascular diseases. Vasculopathy is suggested to be caused by the dysregulation of vascular niches, a microenvironment of vascular structures comprising anatomical structures, extracellular [...] Read more.
The increasing burden of vascular dysfunction on healthcare systems worldwide results in higher morbidity and mortality rates across pathologies, including cardiovascular diseases. Vasculopathy is suggested to be caused by the dysregulation of vascular niches, a microenvironment of vascular structures comprising anatomical structures, extracellular matrix components, and various cell populations. These elements work together to ensure accurate control of the vascular network. In recent years, autophagy has been recognized as a crucial regulator of the vascular microenvironment responsible for maintaining basic cell functions such as proliferation, differentiation, replicative senescence, and apoptosis. Experimental studies indicate that autophagy activation can be enhanced or inhibited in various pathologies associated with vascular dysfunction, suggesting that autophagy plays both beneficial and detrimental roles. Here, we review and assess the principles of autophagy organization and regulation in non-tumor vascular niches. Our analysis focuses on significant figures in the vascular microenvironment, highlighting the role of autophagy and summarizing evidence that supports the systemic or multiorgan nature of the autophagy effects. Finally, we discuss the critical organizational and functional aspects of the vasculogenic niche, specifically in relation to autophagy. The resulting dysregulation of the vascular microenvironment contributes to the development of vascular dysfunction. Full article
(This article belongs to the Special Issue The Role of Autophagy in Disease and Cancer)
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