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Cells
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Advances in Selective Autophagy
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Advances in Selective Autophagy

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

Deadline for manuscript submissions: closed (15 February 2020)

Special Issue Editors

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
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

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 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 degradation of ribosome, xenophagy for degradation of pathogens, pexophagy for degradation of peroxisomes, lipophagy for degradation of lipids, aggrephagy for degradation of protein aggregates, and mitophagy for the degradation of damaged mitochondria. In this special issue, we welcome you to submit your original research or review manuscripts on selective autophagy to this exciting special issue.

Prof. Wen-Xing Ding
Dr. Qiming Sun
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 (7 papers)

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Research

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13 pages, 15209 KiB  
Article
iNOS Interacts with Autophagy Receptor p62 and is Degraded by Autophagy in Macrophages
by Jing Wang, Ming-Yue Wu, Huanxing Su, Jinjian Lu, Xiuping Chen, Jieqiong Tan and Jia-Hong Lu
Cells 2019, 8(10), 1255; https://doi.org/10.3390/cells8101255 - 15 Oct 2019
Cited by 19 | Viewed by 5013
Abstract
Nitric oxide (NO) is an important mediator of inflammation response and the production of NO has been linked to a variety of diseases, including tumors, inflammation and central nervous system diseases. In macrophages, a high level of NO is generated by iNOS during [...] Read more.
Nitric oxide (NO) is an important mediator of inflammation response and the production of NO has been linked to a variety of diseases, including tumors, inflammation and central nervous system diseases. In macrophages, a high level of NO is generated by iNOS during inflammatory responses triggered by cytokines or pathogens. Autophagy, a cellular bulk degradation process via lysosome, has been implicated in many disease conditions including inflammation. In this study, we have reported the previously unknown role of autophagy in regulating iNOS levels in macrophages, both under basal and Lipopolysaccharides (LPS)-induced conditions. Our data showed that iNOS levels accumulated upon autophagy inhibition and decreased upon autophagy induction. iNOS interacted and co-localized with autophagy receptor p62/SQSTM1, especially under LPS-stimulated condition in macrophages. Moreover, the immunostaining data revealed that iNOS also co-localizes with the autophagosome marker LC3 and lysosome marker LAMP1, especially under lysosomal inhibition conditions, indicating iNOS is an autophagy substrate. Finally, we showed that autophagy negatively regulated the generation of NO in macrophages, which is consistent with the changes of iNOS levels. Collectively, our study revealed a previously unknown mechanism by which autophagy regulates iNOS levels to modulate NO production during inflammation. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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Review

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30 pages, 2018 KiB  
Review
Role and Mechanisms of Mitophagy in Liver Diseases
by Xiaowen Ma, Tara McKeen, Jianhua Zhang and Wen-Xing Ding
Cells 2020, 9(4), 837; https://doi.org/10.3390/cells9040837 - 31 Mar 2020
Cited by 144 | Viewed by 14163
Abstract
The mitochondrion is an organelle that plays a vital role in the regulation of hepatic cellular redox, lipid metabolism, and cell death. Mitochondrial dysfunction is associated with both acute and chronic liver diseases with emerging evidence indicating that mitophagy, a selective form of [...] Read more.
The mitochondrion is an organelle that plays a vital role in the regulation of hepatic cellular redox, lipid metabolism, and cell death. Mitochondrial dysfunction is associated with both acute and chronic liver diseases with emerging evidence indicating that mitophagy, a selective form of autophagy for damaged/excessive mitochondria, plays a key role in the liver’s physiology and pathophysiology. This review will focus on mitochondrial dynamics, mitophagy regulation, and their roles in various liver diseases (alcoholic liver disease, non-alcoholic fatty liver disease, drug-induced liver injury, hepatic ischemia-reperfusion injury, viral hepatitis, and cancer) with the hope that a better understanding of the molecular events and signaling pathways in mitophagy regulation will help identify promising targets for the future treatment of liver diseases. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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21 pages, 978 KiB  
Review
Implications of Selective Autophagy Dysfunction for ALS Pathology
by Emiliano Vicencio, Sebastián Beltrán, Luis Labrador, Patricio Manque, Melissa Nassif and Ute Woehlbier
Cells 2020, 9(2), 381; https://doi.org/10.3390/cells9020381 - 07 Feb 2020
Cited by 35 | Viewed by 6717
Abstract
Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disorder that progressively affects motor neurons in the brain and spinal cord. Due to the biological complexity of the disease, its etiology remains unknown. Several cellular mechanisms involved in the neurodegenerative process in ALS have [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disorder that progressively affects motor neurons in the brain and spinal cord. Due to the biological complexity of the disease, its etiology remains unknown. Several cellular mechanisms involved in the neurodegenerative process in ALS have been found, including the loss of RNA and protein homeostasis, as well as mitochondrial dysfunction. Insoluble protein aggregates, damaged mitochondria, and stress granules, which contain RNA and protein components, are recognized and degraded by the autophagy machinery in a process known as selective autophagy. Autophagy is a highly dynamic process whose dysregulation has now been associated with neurodegenerative diseases, including ALS, by numerous studies. In ALS, the autophagy process has been found deregulated in both familial and sporadic cases of the disease. Likewise, mutations in genes coding for proteins involved in the autophagy machinery have been reported in ALS patients, including selective autophagy receptors. In this review, we focus on the role of selective autophagy in ALS pathology. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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18 pages, 1446 KiB  
Review
Mitophagy in Acute Kidney Injury and Kidney Repair
by Ying Wang, Juan Cai, Chengyuan Tang and Zheng Dong
Cells 2020, 9(2), 338; https://doi.org/10.3390/cells9020338 - 01 Feb 2020
Cited by 81 | Viewed by 7504
Abstract
Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of [...] Read more.
Acute kidney injury (AKI) is a major kidney disease characterized by rapid decline of renal function. Besides its acute consequence of high mortality, AKI has recently been recognized as an independent risk factor for chronic kidney disease (CKD). Maladaptive or incomplete repair of renal tubules after severe or episodic AKI leads to renal fibrosis and, eventually, CKD. Recent studies highlight a key role of mitochondrial pathology in AKI development and abnormal kidney repair after AKI. As such, timely elimination of damaged mitochondria in renal tubular cells represents an important quality control mechanism for cell homeostasis and survival during kidney injury and repair. Mitophagy is a selective form of autophagy that selectively removes redundant or damaged mitochondria. Here, we summarize our recent understanding on the molecular mechanisms of mitophagy, discuss the role of mitophagy in AKI development and kidney repair after AKI, and present future research directions and therapeutic potential. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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21 pages, 1886 KiB  
Review
Targeting Aggrephagy for the Treatment of Alzheimer’s Disease
by Sandeep Malampati, Ju-Xian Song, Benjamin Chun-Kit Tong, Anusha Nalluri, Chuan-Bin Yang, Ziying Wang, Sravan Gopalkrishnashetty Sreenivasmurthy, Zhou Zhu, Jia Liu, Chengfu Su, Senthilkumar Krishnamoorthi, Ashok Iyaswamy, King-Ho Cheung, Jia-Hong Lu and Min Li
Cells 2020, 9(2), 311; https://doi.org/10.3390/cells9020311 - 28 Jan 2020
Cited by 29 | Viewed by 6433
Abstract
Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases in older individuals with specific neuropsychiatric symptoms. It is a proteinopathy, pathologically characterized by the presence of misfolded protein (Aβ and Tau) aggregates in the brain, causing progressive dementia. Increasing studies have [...] Read more.
Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases in older individuals with specific neuropsychiatric symptoms. It is a proteinopathy, pathologically characterized by the presence of misfolded protein (Aβ and Tau) aggregates in the brain, causing progressive dementia. Increasing studies have provided evidence that the defect in protein-degrading systems, especially the autophagy-lysosome pathway (ALP), plays an important role in the pathogenesis of AD. Recent studies have demonstrated that AD-associated protein aggregates can be selectively recognized by some receptors and then be degraded by ALP, a process termed aggrephagy. In this study, we reviewed the role of aggrephagy in AD development and discussed the strategy of promoting aggrephagy using small molecules for the treatment of AD. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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25 pages, 1726 KiB  
Review
Autophagy and Macrophage Functions: Inflammatory Response and Phagocytosis
by Ming-Yue Wu and Jia-Hong Lu
Cells 2020, 9(1), 70; https://doi.org/10.3390/cells9010070 - 27 Dec 2019
Cited by 120 | Viewed by 13266
Abstract
Autophagy is a conserved bulk degradation and recycling process that plays important roles in multiple biological functions, including inflammatory responses. As an important component of the innate immune system, macrophages are involved in defending cells from invading pathogens, clearing cellular debris, and regulating [...] Read more.
Autophagy is a conserved bulk degradation and recycling process that plays important roles in multiple biological functions, including inflammatory responses. As an important component of the innate immune system, macrophages are involved in defending cells from invading pathogens, clearing cellular debris, and regulating inflammatory responses. During the past two decades, accumulated evidence has revealed the intrinsic connection between autophagy and macrophage function. This review focuses on the role of autophagy, both as nonselective and selective forms, in the regulation of the inflammatory and phagocytotic functions of macrophages. Specifically, the roles of autophagy in pattern recognition, cytokine release, inflammasome activation, macrophage polarization, LC3-associated phagocytosis, and xenophagy are comprehensively reviewed. The roles of autophagy receptors in the macrophage function regulation are also summarized. Finally, the obstacles and remaining questions regarding the molecular regulation mechanisms, disease association, and therapeutic applications are discussed. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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18 pages, 1811 KiB  
Review
Physical Exercise and Selective Autophagy: Benefit and Risk on Cardiovascular Health
by Ne N. Wu, Haili Tian, Peijie Chen, Dan Wang, Jun Ren and Yingmei Zhang
Cells 2019, 8(11), 1436; https://doi.org/10.3390/cells8111436 - 14 Nov 2019
Cited by 75 | Viewed by 12669
Abstract
Physical exercise promotes cardiorespiratory fitness, and is considered the mainstream of non-pharmacological therapies along with lifestyle modification for various chronic diseases, in particular cardiovascular diseases. Physical exercise may positively affect various cardiovascular risk factors including body weight, blood pressure, insulin sensitivity, lipid and [...] Read more.
Physical exercise promotes cardiorespiratory fitness, and is considered the mainstream of non-pharmacological therapies along with lifestyle modification for various chronic diseases, in particular cardiovascular diseases. Physical exercise may positively affect various cardiovascular risk factors including body weight, blood pressure, insulin sensitivity, lipid and glucose metabolism, heart function, endothelial function, and body fat composition. With the ever-rising prevalence of obesity and other types of metabolic diseases, as well as sedentary lifestyle, regular exercise of moderate intensity has been indicated to benefit cardiovascular health and reduce overall disease mortality. Exercise offers a wide cadre of favorable responses in the cardiovascular system such as improved dynamics of the cardiovascular system, reduced prevalence of coronary heart diseases and cardiomyopathies, enhanced cardiac reserve capacity, and autonomic regulation. Ample clinical and experimental evidence has indicated an emerging role for autophagy, a conservative catabolism process to degrade and recycle cellular organelles and nutrients, in exercise training-offered cardiovascular benefits. Regular physical exercise as a unique form of physiological stress is capable of triggering adaptation while autophagy in particular selective autophagy seems to be permissive to such cardiovascular adaptation. Here in this mini-review, we will summarize the role for autophagy in particular mitochondrial selective autophagy namely mitophagy in the benefit versus risk of physical exercise on cardiovascular function. Full article
(This article belongs to the Special Issue Advances in Selective Autophagy)
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