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Advances in Selective Autophagy - Series 2
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Advances in Selective Autophagy - Series 2

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

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 32486

Special Issue Editors

Prof. Dr. Qiming Sun

E-Mail Website
Guest Editor
Department of Biochemistry and Genetics, Zhejiang University School of Medicine, Hangzhou, China
Interests: autophagy; organelle-interaction network
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Wen-Xing Ding

E-Mail Website
Guest Editor
Department of Pharmacology, Toxicology, and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA
Interests: alcohol; autophagy; liver disease; lysosome; mitochondria
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is an evolutionarily conserved catabolic process that degrades cellular proteins and damaged/or excess organelles through the formation of a double-membrane autophagosome. In 2016, Professor Yoshinori Ohsumi was awarded the Nobel Prize in Physiology or Medicine for his discoveries of the autophagy-related (Atg) genes in regulating autophagy in yeast, which are also conserved in mammalian cells. Now, the research in autophagy has been expanded exponentially due to the advancement of the understanding of the molecular mechanisms on how autophagy is regulated. Autophagy can be both a non-selective and a selective process. Selective autophagy removes damaged organelles and protein aggregates as well as invading pathogens using specific receptors. So far, many forms of selective autophagy have been reported, including ERphagy for endoplasmic reticulum degradation, ribophagy for ribosome degradation, xenophagy for the degradation of pathogens, pexophagy for the degradation of peroxisomes, lipophagy for the degradation of lipids, aggrephagy for the degradation of protein aggregates, and mitophagy for the degradation of damaged mitochondria. Although great progress has been made in the selective autophagy field, many critical questions remain to be addressed. For instance, what are the uncharacterized selective autophagy cargoes and their receptors? How do selective autophagy receptors sense upstream signals to initiate the autophagic elimination of their targets? What are the physiological and pathological functions of different selective autophagy in different cell types, organs, or tissues? How can we translate our current understanding of selective autophagy to find cures for different human diseases, especially for neurodegenerative diseases? In this Special Issue, we welcome you to submit your original research or review manuscripts on selective autophagy to this exciting Special Issue.

Dr. Qiming Sun
Prof. Wen-Xing Ding
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. 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

  • autophagy
  • erphagy
  • lipophagy
  • mitophagy
  • xenophagy
  • liver
  • kidney
  • heart
  • neurodegeneration

Published Papers (8 papers)

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Research

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16 pages, 2820 KiB  
Article
The Autophagy Protein Pacer Positively Regulates the Therapeutic Potential of Mesenchymal Stem Cells in a Mouse Model of DSS-Induced Colitis
by Cristian A. Bergmann, Sebastian Beltran, Ana Maria Vega-Letter, Paola Murgas, Maria Fernanda Hernandez, Laura Gomez, Luis Labrador, Bastián I. Cortés, Cristian Poblete, Cristobal Quijada, Flavio Carrion, Ute Woehlbier and Patricio A. Manque
Cells 2022, 11(9), 1503; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11091503 - 30 Apr 2022
Cited by 6 | Viewed by 2614
Abstract
Mesenchymal stem cells (MSC) have emerged as a promising tool to treat inflammatory diseases, such as inflammatory bowel disease (IBD), due to their immunoregulatory properties. Frequently, IBD is modeled in mice by using dextran sulfate sodium (DSS)-induced colitis. Recently, the modulation of autophagy [...] Read more.
Mesenchymal stem cells (MSC) have emerged as a promising tool to treat inflammatory diseases, such as inflammatory bowel disease (IBD), due to their immunoregulatory properties. Frequently, IBD is modeled in mice by using dextran sulfate sodium (DSS)-induced colitis. Recently, the modulation of autophagy in MSC has been suggested as a novel strategy to improve MSC-based immunotherapy. Hence, we investigated a possible role of Pacer, a novel autophagy enhancer, in regulating the immunosuppressive function of MSC in the context of DSS-induced colitis. We found that Pacer is upregulated upon stimulation with the pro-inflammatory cytokine TNFα, the main cytokine released in the inflammatory environment of IBD. By modulating Pacer expression in MSC, we found that Pacer plays an important role in regulating the autophagy pathway in this cell type in response to TNFα stimulation, as well as in regulating the immunosuppressive ability of MSC toward T-cell proliferation. Furthermore, increased expression of Pacer in MSC enhanced their ability to ameliorate the symptoms of DSS-induced colitis in mice. Our results support previous findings that autophagy regulates the therapeutic potential of MSC and suggest that the augmentation of autophagic capacity in MSC by increasing Pacer levels may have therapeutic implications for IBD. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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15 pages, 4770 KiB  
Article
Aging-Related Changes in the Ultrastructure of Hepatocytes and Cardiomyocytes of Elderly Mice Are Enhanced in ApoE-Deficient Animals
by Małgorzata Łysek-Gładysińska, Anna Wieczorek, Artur Jóźwik, Anna Walaszczyk, Karol Jelonek, Grażyna Szczukiewicz-Markowska, Olaf K. Horbańczuk, Monika Pietrowska, Piotr Widłak and Dorota Gabryś
Cells 2021, 10(3), 502; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10030502 - 26 Feb 2021
Cited by 8 | Viewed by 2217
Abstract
Biological aging is associated with various morphological and functional changes, yet the mechanisms of these phenomena remain unclear in many tissues and organs. Hyperlipidemia is among the factors putatively involved in the aging of the liver and heart. Here, we analyzed morphological, ultrastructural, [...] Read more.
Biological aging is associated with various morphological and functional changes, yet the mechanisms of these phenomena remain unclear in many tissues and organs. Hyperlipidemia is among the factors putatively involved in the aging of the liver and heart. Here, we analyzed morphological, ultrastructural, and biochemical features in adult (7-month-old) and elderly (17-month-old) mice, and then compared age-related features between wild type (C57Bl/6 strain) and ApoE-deficient (transgenic ApoE−/−) animals. Increased numbers of damaged mitochondria, lysosomes, and lipid depositions were observed in the hepatocytes of elderly animals. Importantly, these aging-related changes were significantly stronger in hepatocytes from ApoE-deficient animals. An increased number of damaged mitochondria was observed in the cardiomyocytes of elderly animals. However, the difference between wild type and ApoE-deficient mice was expressed in the larger size of mitochondria detected in the transgenic animals. Moreover, a few aging-related differences were noted between wild type and ApoE-deficient mice at the level of plasma biochemical markers. Levels of cholesterol and HDL increased in the plasma of elderly ApoE−/− mice and were markedly higher than in the plasma of elderly wild type animals. On the other hand, the activity of alanine transaminase (ALT) decreased in the plasma of elderly ApoE−/− mice and was markedly lower than in the plasma of elderly wild type animals. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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Review

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13 pages, 1480 KiB  
Review
Key Regulators of Autophagosome Closure
by Wenyan Jiang, Xuechai Chen, Cuicui Ji, Wenting Zhang, Jianing Song, Jie Li and Juan Wang
Cells 2021, 10(11), 2814; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10112814 - 20 Oct 2021
Cited by 16 | Viewed by 3231
Abstract
Autophagy is an evolutionarily conserved pathway, in which cytoplasmic components are sequestered within double-membrane vesicles called autophagosomes and then transported into lysosomes or vacuoles for degradation. Over 40 conserved autophagy-related (ATG) genes define the core machinery for the five processes of autophagy: initiation, [...] Read more.
Autophagy is an evolutionarily conserved pathway, in which cytoplasmic components are sequestered within double-membrane vesicles called autophagosomes and then transported into lysosomes or vacuoles for degradation. Over 40 conserved autophagy-related (ATG) genes define the core machinery for the five processes of autophagy: initiation, nucleation, elongation, closure, and fusion. In this review, we focus on one of the least well-characterized events in autophagy, namely the closure of the isolation membrane/phagophore to form the sealed autophagosome. This process is tightly regulated by ESCRT machinery, ATG proteins, Rab GTPase and Rab-related proteins, SNAREs, sphingomyelin, and calcium. We summarize recent progress in the regulation of autophagosome closure and discuss the key questions remaining to be addressed. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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25 pages, 1657 KiB  
Review
Advances in ER-Phagy and Its Diseases Relevance
by Lingang He, Xuehong Qian and Yixian Cui
Cells 2021, 10(9), 2328; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092328 - 06 Sep 2021
Cited by 14 | Viewed by 5928
Abstract
As an important form of selective autophagy in cells, ER-phagy (endoplasmic reticulum-selective autophagy), the autophagic degradation of endoplasmic reticulum (ER), degrades ER membranes and proteins to maintain cellular homeostasis. The relationship between ER-phagy and human diseases, including neurodegenerative disorders, cancer, and other metabolic [...] Read more.
As an important form of selective autophagy in cells, ER-phagy (endoplasmic reticulum-selective autophagy), the autophagic degradation of endoplasmic reticulum (ER), degrades ER membranes and proteins to maintain cellular homeostasis. The relationship between ER-phagy and human diseases, including neurodegenerative disorders, cancer, and other metabolic diseases has been unveiled by extensive research in recent years. Starting with the catabolic process of ER-phagy and key mediators in this pathway, this paper reviews the advances in the mechanism of ER-phagy and its diseases relevance. We hope to provide some enlightenment for further study on ER-phagy and the development of novel therapeutic strategies for related diseases. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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13 pages, 537 KiB  
Review
Aberrant Stress Granule Dynamics and Aggrephagy in ALS Pathogenesis
by Yi Zhang, Jiayu Gu and Qiming Sun
Cells 2021, 10(9), 2247; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092247 - 30 Aug 2021
Cited by 16 | Viewed by 4018
Abstract
Stress granules are conserved cytosolic ribonucleoprotein (RNP) compartments that undergo dynamic assembly and disassembly by phase separation in response to stressful conditions. Gene mutations may lead to aberrant phase separation of stress granules eliciting irreversible protein aggregations. A selective autophagy pathway called aggrephagy [...] Read more.
Stress granules are conserved cytosolic ribonucleoprotein (RNP) compartments that undergo dynamic assembly and disassembly by phase separation in response to stressful conditions. Gene mutations may lead to aberrant phase separation of stress granules eliciting irreversible protein aggregations. A selective autophagy pathway called aggrephagy may partially alleviate the cytotoxicity mediated by these protein aggregates. Cells must perceive when and where the stress granules are transformed into toxic protein aggregates to initiate autophagosomal engulfment for subsequent autolysosomal degradation, therefore, maintaining cellular homeostasis. Indeed, defective aggrephagy has been causally linked to various neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). In this review, we discuss stress granules at the intersection of autophagy and ALS pathogenesis. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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16 pages, 2372 KiB  
Review
Oligomerization of Selective Autophagy Receptors for the Targeting and Degradation of Protein Aggregates
by Wenjun Chen, Tianyun Shen, Lijun Wang and Kefeng Lu
Cells 2021, 10(8), 1989; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10081989 - 05 Aug 2021
Cited by 8 | Viewed by 3785
Abstract
The selective targeting and disposal of solid protein aggregates are essential for cells to maintain protein homoeostasis. Autophagy receptors including p62, NBR1, Cue5/TOLLIP (CUET), and Tax1-binding protein 1 (TAX1BP1) proteins function in selective autophagy by targeting ubiquitinated aggregates through ubiquitin-binding domains. Here, we [...] Read more.
The selective targeting and disposal of solid protein aggregates are essential for cells to maintain protein homoeostasis. Autophagy receptors including p62, NBR1, Cue5/TOLLIP (CUET), and Tax1-binding protein 1 (TAX1BP1) proteins function in selective autophagy by targeting ubiquitinated aggregates through ubiquitin-binding domains. Here, we summarize previous beliefs and recent findings on selective receptors in aggregate autophagy. Since there are many reviews on selective autophagy receptors, we focus on their oligomerization, which enables receptors to function as pathway determinants and promotes phase separation. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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16 pages, 480 KiB  
Review
Mitophagy Regulates Neurodegenerative Diseases
by Xufeng Cen, Manke Zhang, Mengxin Zhou, Lingzhi Ye and Hongguang Xia
Cells 2021, 10(8), 1876; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10081876 - 24 Jul 2021
Cited by 25 | Viewed by 4572
Abstract
Mitochondria play an essential role in supplying energy for the health and survival of neurons. Mitophagy is a metabolic process that removes dysfunctional or redundant mitochondria. This process preserves mitochondrial health. However, defective mitophagy triggers the accumulation of damaged mitochondria, causing major neurodegenerative [...] Read more.
Mitochondria play an essential role in supplying energy for the health and survival of neurons. Mitophagy is a metabolic process that removes dysfunctional or redundant mitochondria. This process preserves mitochondrial health. However, defective mitophagy triggers the accumulation of damaged mitochondria, causing major neurodegenerative disorders. This review introduces molecular mechanisms and signaling pathways behind mitophagy regulation. Furthermore, we focus on the recent advances in understanding the potential role of mitophagy in the pathogenesis of major neurodegenerative diseases (Parkinson’s, Alzheimer’s, Huntington’s, etc.) and aging. The findings will help identify the potential interventions of mitophagy regulation and treatment strategies of neurodegenerative diseases. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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14 pages, 1084 KiB  
Review
Mechanisms and Functions of Pexophagy in Mammalian Cells
by Jing Li and Wei Wang
Cells 2021, 10(5), 1094; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10051094 - 03 May 2021
Cited by 17 | Viewed by 4897
Abstract
Peroxisomes play essential roles in diverse cellular metabolism functions, and their dynamic homeostasis is maintained through the coordination of peroxisome biogenesis and turnover. Pexophagy, selective autophagic degradation of peroxisomes, is a major mechanism for removing damaged and/or superfluous peroxisomes. Dysregulation of pexophagy impairs [...] Read more.
Peroxisomes play essential roles in diverse cellular metabolism functions, and their dynamic homeostasis is maintained through the coordination of peroxisome biogenesis and turnover. Pexophagy, selective autophagic degradation of peroxisomes, is a major mechanism for removing damaged and/or superfluous peroxisomes. Dysregulation of pexophagy impairs the physiological functions of peroxisomes and contributes to the progression of many human diseases. However, the mechanisms and functions of pexophagy in mammalian cells remain largely unknown compared to those in yeast. This review focuses on mammalian pexophagy and aims to advance the understanding of the roles of pexophagy in human health and diseases. Increasing evidence shows that ubiquitination can serve as a signal for pexophagy, and ubiquitin-binding receptors, substrates, and E3 ligases/deubiquitinases involved in pexophagy have been described. Alternatively, pexophagy can be achieved in a ubiquitin-independent manner. We discuss the mechanisms of these ubiquitin-dependent and ubiquitin-independent pexophagy pathways and summarize several inducible conditions currently used to study pexophagy. We highlight several roles of pexophagy in human health and how its dysregulation may contribute to diseases. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy - Series 2)
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