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Autophagy, Mitophagy and Disease
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Autophagy, Mitophagy and Disease

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

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 9062

Special Issue Editor

Dr. Andreas Till

E-Mail Website
Guest Editor
Department of Internal Medicine I, Division of Endocrinology, Diabetes and Metabolism, University Medical Center Bonn, 53127 Bonn, Germany
Interests: cellular stress pathways; autophagy; mitochondrial homeostasis; neurodegeneration; metabolic diseases; obesity; inflammation; infection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since the introduction of the term ‘autophagy’ for all processes that deliver cytosolic material to the lysosome or vacuole for degradation by Christian de Duve in the 1960s and the identification of the genes that encode for the execution machinery by Yoshinori Ohsumi in the 1980s, this process has taken center stage in basic and translational research. The well-established mechanistic contribution of autophagy (and its selective subtypes, e.g., mitophagy) to human diseases such as neurodegeneration, cancer, and metabolic syndrome has spawned the quest for tailored drugs that target specific regulatory proteins or pathways involved in pathogenic events. In this Special Issue of Cells, I cordially invite you to contribute reviews, comments, or original research articles on various aspects related to the theme of “Autophagy, Mitophagy and Disease”. Articles addressing cellular, biochemical, mechanistic, translational, clinical, or general aspects of autophagy and its selective forms are highly welcome. Relevant topics include but are not limited to:

  • Molecular mechanisms of autophagy and mitophagy
  • Mitochondrial homeostasis
  • Organelle turnover
  • Selective autophagy pathways
  • Clinical relevance of autophagy and mitophagy
  • Molecular mechanisms of regulation and execution
  • Chronic inflammation
  • Cancer
  • Neurodegeneration
  • Mood disorders
  • Infection
  • Intracellular pathogens
  • Metabolic syndrome
  • Autophagic cell death
  • Stem cell biology
  • Aging
  • Drugs targeting autophagy pathways.

This may also be a great opportunity for early-stage researchers to present their data or introduce their view on selected aspects of this fascinating cellular pathway. As a plus, this Special Issue will be made available in printed book format if we jointly manage to publish more than 10 papers.

I look forward to your ideas and contributions!

Dr. Andreas Till
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.

Published Papers (4 papers)

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Research

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14 pages, 4607 KiB  
Article
Glycogen Granules Are Degraded by Non-Selective Autophagy in Nitrogen-Starved Komagataella phaffii
by Nimna V. Wijewantha, Ravinder Kumar and Taras Y. Nazarko
Cells 2024, 13(6), 467; https://doi.org/10.3390/cells13060467 - 07 Mar 2024
Cited by 1 | Viewed by 1921
Abstract
Autophagy was initially recognized as a bulk degradation process that randomly sequesters and degrades cytoplasmic material in lysosomes (vacuoles in yeast). In recent years, various types of selective autophagy have been discovered. Glycophagy, the selective autophagy of glycogen granules, is one of them. [...] Read more.
Autophagy was initially recognized as a bulk degradation process that randomly sequesters and degrades cytoplasmic material in lysosomes (vacuoles in yeast). In recent years, various types of selective autophagy have been discovered. Glycophagy, the selective autophagy of glycogen granules, is one of them. While autophagy of glycogen is an important contributor to Pompe disease, which is characterized by the lysosomal accumulation of glycogen, its selectivity is still a matter of debate. Here, we developed the Komagataella phaffii yeast as a simple model of glycogen autophagy under nitrogen starvation conditions to address the question of its selectivity. For this, we turned the self-glucosylating initiator of glycogen synthesis, Glg1, which is covalently bound to glycogen, into the Glg1-GFP autophagic reporter. Our results revealed that vacuolar delivery of Glg1-GFP and its processing to free GFP were strictly dependent on autophagic machinery and vacuolar proteolysis. Notably, this process was independent of Atg11, the scaffold protein common for many selective autophagy pathways. Importantly, the non-mutated Glg1-GFP (which synthesizes and marks glycogen) and mutated Glg1Y212F-GFP (which does not synthesize glycogen and is degraded by non-selective autophagy as cytosolic Pgk1-GFP) were equally well delivered to the vacuole and had similar levels of released GFP. Therefore, we concluded that glycogen autophagy is a non-selective process in K. phaffii yeast under nitrogen starvation conditions. Full article
(This article belongs to the Special Issue Autophagy, Mitophagy and Disease)
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20 pages, 8180 KiB  
Article
Novel Filamin C Myofibrillar Myopathy Variants Cause Different Pathomechanisms and Alterations in Protein Quality Systems
by Dominik Sellung, Lorena Heil, Nassam Daya, Frank Jacobsen, Janine Mertens-Rill, Heidi Zhuge, Kristina Döring, Misagh Piran, Hendrik Milting, Andreas Unger, Wolfgang A. Linke, Rudi Kley, Corinna Preusse, Andreas Roos, Dieter O. Fürst, Peter F. M. van der Ven and Matthias Vorgerd
Cells 2023, 12(9), 1321; https://doi.org/10.3390/cells12091321 - 05 May 2023
Cited by 2 | Viewed by 2174
Abstract
Myofibrillar myopathies (MFM) are a group of chronic muscle diseases pathophysiologically characterized by accumulation of protein aggregates and structural failure of muscle fibers. A subtype of MFM is caused by heterozygous mutations in the filamin C (FLNC) gene, exhibiting progressive muscle [...] Read more.
Myofibrillar myopathies (MFM) are a group of chronic muscle diseases pathophysiologically characterized by accumulation of protein aggregates and structural failure of muscle fibers. A subtype of MFM is caused by heterozygous mutations in the filamin C (FLNC) gene, exhibiting progressive muscle weakness, muscle structural alterations and intracellular protein accumulations. Here, we characterize in depth the pathogenicity of two novel truncating FLNc variants (p.Q1662X and p.Y2704X) and assess their distinct effect on FLNc stability and distribution as well as their impact on protein quality system (PQS) pathways. Both variants cause a slowly progressive myopathy with disease onset in adulthood, chronic myopathic alterations in muscle biopsy including the presence of intracellular protein aggregates. Our analyses revealed that p.Q1662X results in FLNc haploinsufficiency and p.Y2704X in a dominant-negative FLNc accumulation. Moreover, both protein-truncating variants cause different PQS alterations: p.Q1662X leads to an increase in expression of several genes involved in the ubiquitin-proteasome system (UPS) and the chaperone-assisted selective autophagy (CASA) system, whereas p.Y2704X results in increased abundance of proteins involved in UPS activation and autophagic buildup. We conclude that truncating FLNC variants might have different pathogenetic consequences and impair PQS function by diverse mechanisms and to varying extents. Further studies on a larger number of patients are necessary to confirm our observations. Full article
(This article belongs to the Special Issue Autophagy, Mitophagy and Disease)
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Review

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26 pages, 1450 KiB  
Review
Unraveling the Intricacies of Autophagy and Mitophagy: Implications in Cancer Biology
by Sunmi Lee, Ji-Yoon Son, Jinkyung Lee and Heesun Cheong
Cells 2023, 12(23), 2742; https://doi.org/10.3390/cells12232742 - 30 Nov 2023
Viewed by 2193
Abstract
Autophagy is an essential lysosome-mediated degradation pathway that maintains cellular homeostasis and viability in response to various intra- and extracellular stresses. Mitophagy is a type of autophagy that is involved in the intricate removal of dysfunctional mitochondria during conditions of metabolic stress. In [...] Read more.
Autophagy is an essential lysosome-mediated degradation pathway that maintains cellular homeostasis and viability in response to various intra- and extracellular stresses. Mitophagy is a type of autophagy that is involved in the intricate removal of dysfunctional mitochondria during conditions of metabolic stress. In this review, we describe the multifaceted roles of autophagy and mitophagy in normal physiology and the field of cancer biology. Autophagy and mitophagy exhibit dual context-dependent roles in cancer development, acting as tumor suppressors and promoters. We also discuss the important role of autophagy and mitophagy within the cancer microenvironment and how autophagy and mitophagy influence tumor host–cell interactions to overcome metabolic deficiencies and sustain the activity of cancer-associated fibroblasts (CAFs) in a stromal environment. Finally, we explore the dynamic interplay between autophagy and the immune response in tumors, indicating their potential as immunomodulatory targets in cancer therapy. As the field of autophagy and mitophagy continues to evolve, this comprehensive review provides insights into their important roles in cancer and cancer microenvironment. Full article
(This article belongs to the Special Issue Autophagy, Mitophagy and Disease)
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18 pages, 780 KiB  
Review
Autophagy in Crohn’s Disease: Converging on Dysfunctional Innate Immunity
by Kibrom M. Alula and Arianne L. Theiss
Cells 2023, 12(13), 1779; https://doi.org/10.3390/cells12131779 - 04 Jul 2023
Cited by 4 | Viewed by 2192
Abstract
Crohn’s disease (CD) is a chronic inflammatory bowel disease marked by relapsing, transmural intestinal inflammation driven by innate and adaptive immune responses. Autophagy is a multi-step process that plays a critical role in maintaining cellular homeostasis by degrading intracellular components, such as damaged [...] Read more.
Crohn’s disease (CD) is a chronic inflammatory bowel disease marked by relapsing, transmural intestinal inflammation driven by innate and adaptive immune responses. Autophagy is a multi-step process that plays a critical role in maintaining cellular homeostasis by degrading intracellular components, such as damaged organelles and invading bacteria. Dysregulation of autophagy in CD is revealed by the identification of several susceptibility genes, including ATG16L1, IRGM, NOD2, LRRK2, ULK1, ATG4, and TCF4, that are involved in autophagy. In this review, the role of altered autophagy in the mucosal innate immune response in the context of CD is discussed, with a specific focus on dendritic cells, macrophages, Paneth cells, and goblet cells. Selective autophagy, such as xenophagy, ERphagy, and mitophagy, that play crucial roles in maintaining intestinal homeostasis in these innate immune cells, are discussed. As our understanding of autophagy in CD pathogenesis evolves, the development of autophagy-targeted therapeutics may benefit subsets of patients harboring impaired autophagy. Full article
(This article belongs to the Special Issue Autophagy, Mitophagy and Disease)
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