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Autophagy in Health, Ageing and Disease 2.0
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Autophagy in Health, Ageing and Disease 2.0

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

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 67863

Special Issue Editors

Prof. Dr. Patrizia Ballerini

E-Mail Website
Guest Editor
1. Department of Neuroscience, Imaging and Clinical Sciences, “G. d’Annunzio” University of Chieti, 66100 Chieti, Italy
2. Center for Research on Aging and Translational Medicine (CeSI-MeT), “G. d’Annunzio” University of Chieti, 66100 Chieti, Italy
Interests: oxidative/nitrosative stress; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Antonia Patruno

E-Mail Website
Guest Editor
Department of Medicine and Aging Science, University “G. D’Annunzio” Chieti-Pescara, Via dei Vestini, 31, 66100 Chieti, Italy
Interests: oxidative/nitrosative stress; cell signalling; tissue repair; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Mirko Pesce

E-Mail Website
Guest Editor
Department of Medicine and Ageing Sciences, University G. d’Annunzio, Chieti-Pescara, Via dei Vestini, 31, 66100 Chieti, Italy
Interests: myokines; autophagy; senescence; biological bases of emotional state; cognitive performance; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is an evolutionarily conserved intracellular catabolic process. It has an essential role in cellular homeostasis, facilitating lysosomal degradation and the recycling of harmful and damaged cytoplasmic components. Autophagy was first discovered as a survival mechanism in yeasts subjected to nutrient deprivation, and since then, studies in several different organisms have established its critical roles in a variety of biological processes ranging from development to aging. Interestingly, autophagy is often found perturbed in age-related disorders such as cancer, diabetes, neurodegenerative diseases, and sarcopenia. Accordingly, autophagy is important for the maintenance of organismal health, which prominently declines with aging.

This Special Issue of the International Journal of Molecular Sciences, “Autophagy in Health, Ageing, and Disease”, will include a selection of original articles and reviews aimed at expanding our understanding of this multifaceted process and providing support for further investigations on the role of autophagy in cellular homeostasis, aging, and disease. In particular, it will contribute to better explaining the complex machinery of autophagy and lead to further investigations on physiological and pathological fields in which the study of this process is still in its infancy. Moreover, studies on the role of autophagy in age-related processes to open new avenues for the development of novel potential anti-aging therapeutic approaches are also welcome.

Prof. Patrizia Ballerini
Prof. Dr. Antonia Patruno
Dr. Mirko Pesce
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
  • Aging
  • Aging diseases
  • Cell survival
  • Inflammation
  • Oxidative stress
  • Signaling pathway
  • Target identification

Published Papers (15 papers)

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Research

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17 pages, 2774 KiB  
Article
The Role of Oxidative Stress and Autophagy in Blue-Light-Induced Damage to the Retinal Pigment Epithelium in Zebrafish In Vitro and In Vivo
by Kai-Chun Cheng, Yun-Tzu Hsu, Wangta Liu, Huey-Lan Huang, Liang-Yu Chen, Chen-Xi He, Shwu-Jiuan Sheu, Kuo-Jen Chen, Po-Yen Lee, Yi-Hsiung Lin and Chien-Chih Chiu
Int. J. Mol. Sci. 2021, 22(3), 1338; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031338 - 29 Jan 2021
Cited by 29 | Viewed by 4726
Abstract
Age-related macular degeneration (AMD) is the progressive degeneration of the retinal pigment epithelium (RPE), retina, and choriocapillaris among elderly individuals and is the leading cause of blindness worldwide. Thus, a better understanding of the underlying mechanisms in retinal tissue activated by blue light [...] Read more.
Age-related macular degeneration (AMD) is the progressive degeneration of the retinal pigment epithelium (RPE), retina, and choriocapillaris among elderly individuals and is the leading cause of blindness worldwide. Thus, a better understanding of the underlying mechanisms in retinal tissue activated by blue light exposure is important for developing novel treatment and intervention strategies. In this study, blue-light-emitting diodes with a wavelength of 440 nm were applied to RPE cells at a dose of 3.7 ± 0.75 mW/cm2 for 24 h. ARPE-19 cells were used to investigate the underlying mechanism induced by blue light exposure. A trypan blue exclusion assay was used for the cell viability determination. Flow cytometry was used for apoptosis rate detection and autophagy analysis. An immunofluorescence microscopy analysis was used to investigate cellular oxidative stress and DNA damage using DCFDA fluorescence staining and an anti-γH2AX antibody. Blue light exposure of zebrafish larvae was established to investigate the effect on retinal tissue development in vivo. To further demonstrate the comprehensive effect of blue light on ARPE-19 cells, next-generation sequencing (NGS) was performed for an ingenuity pathway analysis (IPA) to reveal additional related mechanisms. The results showed that blue light exposure caused a decrease in cell proliferation and an increase in apoptosis in ARPE-19 cells in a time-dependent manner. Oxidative stress increased during the early stage of 2 h of exposure and activated DNA damage in ARPE-19 cells after 8 h. Furthermore, autophagy was activated in response to blue light exposure at 24–48 h. The zebrafish larvae model showed the unfavorable effect of blue light in prohibiting retinal tissue development. The RNA-Seq results confirmed that blue light induced cell death and participated in tissue growth inhibition and maturation. The current study reveals the mechanisms by which blue light induces cell death in a time-dependent manner. Moreover, both the in vivo and NGS data uncovered blue light’s effect on retinal tissue development, suggesting that exposing children to blue light could be relatively dangerous. These results could benefit the development of preventive strategies utilizing herbal medicine-based treatments for eye diseases or degeneration in the future. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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19 pages, 2071 KiB  
Article
Acute Increases in Intracellular Zinc Lead to an Increased Lysosomal and Mitochondrial Autophagy and Subsequent Cell Demise in Malignant Melanoma
by Emil Rudolf and Kamil Rudolf
Int. J. Mol. Sci. 2021, 22(2), 667; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020667 - 11 Jan 2021
Cited by 7 | Viewed by 2268
Abstract
Changes in zinc content and dysregulated zinc homeostatic mechanisms have been recognized in several solid malignancies such as prostate cancer, breast cancer, or pancreatic cancer. Moreover, it has been shown that zinc serum and/or tissue levels are altered in melanoma with varying effects [...] Read more.
Changes in zinc content and dysregulated zinc homeostatic mechanisms have been recognized in several solid malignancies such as prostate cancer, breast cancer, or pancreatic cancer. Moreover, it has been shown that zinc serum and/or tissue levels are altered in melanoma with varying effects on melanoma development and biology. This study was conducted to explore the effects of acute increases of intracellular zinc in a set of melanoma tissue explants obtained from clinical samples. Measurements of their zinc content showed an extant heterogeneity in total and free intracellular zinc pools associated with varying biological behavior of individual cells, e.g., autophagy levels and propensity to cell death. Use of zinc pyrithione elevated intracellular zinc in a short time frame which resulted in marked changes in mitochondrial activity and lysosomes. These alterations were accompanied by significantly enhanced autophagy flux and subsequent cell demise in the absence of typical apoptotic cell death markers. The present results show for the first time that acutely increased intracellular zinc in melanoma cells specifically enhances their autophagic activity via mitochondria and lysosomes which leads to autophagic cell death. While biologically relevant, this discovery may contribute to our understanding and exploration of zinc in relation to autophagy as a means of controlling melanoma growth and survival. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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13 pages, 2901 KiB  
Article
Axon Injury-Induced Autophagy Activation Is Impaired in a C. elegans Model of Tauopathy
by Su-Hyuk Ko, Gilberto Gonzalez, Zhijie Liu and Lizhen Chen
Int. J. Mol. Sci. 2020, 21(22), 8559; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228559 - 13 Nov 2020
Cited by 5 | Viewed by 2083
Abstract
Autophagy is a conserved pathway that plays a key role in cell homeostasis in normal settings, as well as abnormal and stress conditions. Autophagy dysfunction is found in various neurodegenerative diseases, although it remains unclear whether autophagy impairment is a contributor or consequence [...] Read more.
Autophagy is a conserved pathway that plays a key role in cell homeostasis in normal settings, as well as abnormal and stress conditions. Autophagy dysfunction is found in various neurodegenerative diseases, although it remains unclear whether autophagy impairment is a contributor or consequence of neurodegeneration. Axonal injury is an acute neuronal stress that triggers autophagic responses in an age-dependent manner. In this study, we investigate the injury-triggered autophagy response in a C. elegans model of tauopathy. We found that transgenic expression of pro-aggregant Tau, but not the anti-aggregant Tau, abolished axon injury-induced autophagy activation, resulting in a reduced axon regeneration capacity. Furthermore, axonal trafficking of autophagic vesicles were significantly reduced in the animals expressing pro-aggregant F3ΔK280 Tau, indicating that Tau aggregation impairs autophagy regulation. Importantly, the reduced number of total or trafficking autophagic vesicles in the tauopathy model was not restored by the autophagy activator rapamycin. Loss of PTL-1, the sole Tau homologue in C. elegans, also led to impaired injury-induced autophagy activation, but with an increased basal level of autophagic vesicles. Therefore, we have demonstrated that Tau aggregation as well as Tau depletion both lead to disruption of injury-induced autophagy responses, suggesting that aberrant protein aggregation or microtubule dysfunction can modulate autophagy regulation in neurons after injury. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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15 pages, 4488 KiB  
Article
Age-Related Hearing Loss in C57BL/6J Mice Is Associated with Mitophagy Impairment in the Central Auditory System
by Cha Kyung Youn, Yonghyun Jun, Eu-Ri Jo and Sung Il Cho
Int. J. Mol. Sci. 2020, 21(19), 7202; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21197202 - 29 Sep 2020
Cited by 21 | Viewed by 3104
Abstract
Aging is associated with functional and morphological changes in the sensory organs, including the auditory system. Mitophagy, a process that regulates the turnover of dysfunctional mitochondria, is impaired with aging. This study aimed to investigate the effect of aging on mitophagy in the [...] Read more.
Aging is associated with functional and morphological changes in the sensory organs, including the auditory system. Mitophagy, a process that regulates the turnover of dysfunctional mitochondria, is impaired with aging. This study aimed to investigate the effect of aging on mitophagy in the central auditory system using an age-related hearing loss mouse model. C57BL/6J mice were divided into the following four groups based on age: 1-, 6-, 12-, and 18-month groups. The hearing ability was evaluated by measuring the auditory brainstem response (ABR) thresholds. The mitochondrial DNA damage level and the expression of mitophagy-related genes, and proteins were investigated by real-time polymerase chain reaction and Western blot analyses. The colocalization of mitophagosomes and lysosomes in the mouse auditory cortex and inferior colliculus was analyzed by immunofluorescence analysis. The expression of genes involved in mitophagy, such as PINK1, Parkin, and BNIP3 in the mouse auditory cortex and inferior colliculus, was investigated by immunohistochemical staining. The ABR threshold increased with aging. In addition to the mitochondrial DNA integrity, the mRNA levels of PINK1, Parkin, NIX, and BNIP3, as well as the protein levels of PINK1, Parkin, BNIP3, COX4, LC3B, mitochondrial oxidative phosphorylation (OXPHOS) subunits I–IV in the mouse auditory cortex significantly decreased with aging. The immunofluorescence analysis revealed that the colocalization of mitophagosomes and lysosomes in the mouse auditory cortex and inferior colliculus decreased with aging. The immunohistochemical analysis revealed that the expression of PINK1, Parkin, and BNIP3 decreased in the mouse auditory cortex and inferior colliculus with aging. These findings indicate that aging-associated impaired mitophagy may contribute to the cellular changes observed in an aged central auditory system, which result in age-related hearing loss. Thus, the induction of mitophagy can be a potential therapeutic strategy for age-related hearing loss. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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20 pages, 2589 KiB  
Article
Sestrin2 Phosphorylation by ULK1 Induces Autophagic Degradation of Mitochondria Damaged by Copper-Induced Oxidative Stress
by Heejeong Kim, Byeong Tak Jeon, Isaac M. Kim, Sydney J. Bennett, Carolyn M. Lorch, Martonio Ponte Viana, Jacob F. Myers, Caroline J. Trupp, Zachary T. Whipps, Mondira Kundu, Soonkyu Chung, Xinghui Sun, Oleh Khalimonchuk, Jaekwon Lee and Seung-Hyun Ro
Int. J. Mol. Sci. 2020, 21(17), 6130; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176130 - 25 Aug 2020
Cited by 15 | Viewed by 3986
Abstract
Selective autolysosomal degradation of damaged mitochondria, also called mitophagy, is an indispensable process for maintaining integrity and homeostasis of mitochondria. One well-established mechanism mediating selective removal of mitochondria under relatively mild mitochondria-depolarizing stress is PINK1-Parkin-mediated or ubiquitin-dependent mitophagy. However, additional mechanisms such as [...] Read more.
Selective autolysosomal degradation of damaged mitochondria, also called mitophagy, is an indispensable process for maintaining integrity and homeostasis of mitochondria. One well-established mechanism mediating selective removal of mitochondria under relatively mild mitochondria-depolarizing stress is PINK1-Parkin-mediated or ubiquitin-dependent mitophagy. However, additional mechanisms such as LC3-mediated or ubiquitin-independent mitophagy induction by heavy environmental stress exist and remain poorly understood. The present study unravels a novel role of stress-inducible protein Sestrin2 in degradation of mitochondria damaged by transition metal stress. By utilizing proteomic methods and studies in cell culture and rodent models, we identify autophagy kinase ULK1-mediated phosphorylation sites of Sestrin2 and demonstrate Sestrin2 association with mitochondria adaptor proteins in HEK293 cells. We show that Ser-73 and Ser-254 residues of Sestrin2 are phosphorylated by ULK1, and a pool of Sestrin2 is strongly associated with mitochondrial ATP5A in response to Cu-induced oxidative stress. Subsequently, this interaction promotes association with LC3-coated autolysosomes to induce degradation of mitochondria damaged by Cu-induced ROS. Treatment of cells with antioxidants or a Cu chelator significantly reduces Sestrin2 association with mitochondria. These results highlight the ULK1-Sestrin2 pathway as a novel stress-sensing mechanism that can rapidly induce autophagic degradation of mitochondria under severe heavy metal stress. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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9 pages, 1772 KiB  
Article
Flavopereirine Inhibits Autophagy via the AKT/p38 MAPK Signaling Pathway in MDA-MB-231 Cells
by Ming-Shan Chen, Hsuan-Te Yeh, Yi-Zhen Li, Wen-Chun Lin, Ying-Ray Lee, Ya-Shih Tseng and Shew-Meei Sheu
Int. J. Mol. Sci. 2020, 21(15), 5362; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21155362 - 28 Jul 2020
Cited by 10 | Viewed by 3431
Abstract
Autophagy is a potential target for the treatment of triple negative breast cancer (TNBC). Because of a lack of targeted therapies for TNBC, it is vital to find optimal agents that avoid chemoresistance and metastasis. Flavopereirine has anti-proliferation ability in cancer cells, but [...] Read more.
Autophagy is a potential target for the treatment of triple negative breast cancer (TNBC). Because of a lack of targeted therapies for TNBC, it is vital to find optimal agents that avoid chemoresistance and metastasis. Flavopereirine has anti-proliferation ability in cancer cells, but whether it regulates autophagy in breast cancer cells remains unclear. A Premo™ Tandem Autophagy Sensor Kit was used to image the stage at which flavopereirine affects autophagy by confocal microscopy. A plasmid that constitutively expresses p-AKT and siRNA targeting p38 mitogen-activated protein kinase (MAPK) was used to confirm the related signaling pathways by Western blot. We found that flavopereirine induced microtubule-associated protein 1 light chain 3 (LC3)-II accumulation in a dose- and time-dependent manner in MDA-MB-231 cells. Confocal florescent images showed that flavopereirine blocked autophagosome fusion with lysosomes. Western blotting showed that flavopereirine directly suppressed p-AKT levels and mammalian target of rapamycin (mTOR) translation. Recovery of AKT phosphorylation decreased the level of p-p38 MAPK and LC3-II, but not mTOR. Moreover, flavopereirine-induced LC3-II accumulation was partially reduced in MDA-MB-231 cells that were transfected with p38 MAPK siRNA. Overall, flavopereirine blocked autophagy via LC3-II accumulation in autophagosomes, which was mediated by the AKT/p38 MAPK signaling pathway. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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25 pages, 6213 KiB  
Article
Mechanisms of Action of Autophagy Modulators Dissected by Quantitative Systems Pharmacology Analysis
by Qingya Shi, Fen Pei, Gary A. Silverman, Stephen C. Pak, David H. Perlmutter, Bing Liu and Ivet Bahar
Int. J. Mol. Sci. 2020, 21(8), 2855; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21082855 - 19 Apr 2020
Cited by 19 | Viewed by 6222
Abstract
Autophagy plays an essential role in cell survival/death and functioning. Modulation of autophagy has been recognized as a promising therapeutic strategy against diseases/disorders associated with uncontrolled growth or accumulation of biomolecular aggregates, organelles, or cells including those caused by cancer, aging, neurodegeneration, and [...] Read more.
Autophagy plays an essential role in cell survival/death and functioning. Modulation of autophagy has been recognized as a promising therapeutic strategy against diseases/disorders associated with uncontrolled growth or accumulation of biomolecular aggregates, organelles, or cells including those caused by cancer, aging, neurodegeneration, and liver diseases such as α1-antitrypsin deficiency. Numerous pharmacological agents that enhance or suppress autophagy have been discovered. However, their molecular mechanisms of action are far from clear. Here, we collected a set of 225 autophagy modulators and carried out a comprehensive quantitative systems pharmacology (QSP) analysis of their targets using both existing databases and predictions made by our machine learning algorithm. Autophagy modulators include several highly promiscuous drugs (e.g., artenimol and olanzapine acting as activators, fostamatinib as an inhibitor, or melatonin as a dual-modulator) as well as selected drugs that uniquely target specific proteins (~30% of modulators). They are mediated by three layers of regulation: (i) pathways involving core autophagy-related (ATG) proteins such as mTOR, AKT, and AMPK; (ii) upstream signaling events that regulate the activity of ATG pathways such as calcium-, cAMP-, and MAPK-signaling pathways; and (iii) transcription factors regulating the expression of ATG proteins such as TFEB, TFE3, HIF-1, FoxO, and NF-κB. Our results suggest that PKA serves as a linker, bridging various signal transduction events and autophagy. These new insights contribute to a better assessment of the mechanism of action of autophagy modulators as well as their side effects, development of novel polypharmacological strategies, and identification of drug repurposing opportunities. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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Review

Jump to: Research, Other

15 pages, 1692 KiB  
Review
Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases
by Silvia Vega-Rubín-de-Celis, Lisa Kinch and Samuel Peña-Llopis
Int. J. Mol. Sci. 2020, 21(23), 9210; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21239210 - 03 Dec 2020
Cited by 30 | Viewed by 3452
Abstract
Beclin 1 is a major regulator of autophagy, and it is a core component of the class III PI3K complexes. Beclin 1 is a highly conserved protein and its function is regulated in a number of ways, including post-translational modifications. Several studies indicate [...] Read more.
Beclin 1 is a major regulator of autophagy, and it is a core component of the class III PI3K complexes. Beclin 1 is a highly conserved protein and its function is regulated in a number of ways, including post-translational modifications. Several studies indicate that receptor and non-receptor tyrosine kinases regulate autophagy activity in cancer, and some suggest the importance of Beclin 1 tyrosine phosphorylation in this process. Here we summarize the current knowledge of the mechanism whereby some oncogenic tyrosine kinases regulate autophagy through Beclin 1. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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21 pages, 1044 KiB  
Review
Autophagy and Autophagy-Related Diseases: A Review
by Tadashi Ichimiya, Tsukasa Yamakawa, Takehiro Hirano, Yoshihiro Yokoyama, Yuki Hayashi, Daisuke Hirayama, Kohei Wagatsuma, Takao Itoi and Hiroshi Nakase
Int. J. Mol. Sci. 2020, 21(23), 8974; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21238974 - 26 Nov 2020
Cited by 145 | Viewed by 10380
Abstract
Autophagy refers to the process involving the decomposition of intracellular components via lysosomes. Autophagy plays an important role in maintaining and regulating cell homeostasis by degrading intracellular components and providing degradation products to cells. In vivo, autophagy has been shown to be involved [...] Read more.
Autophagy refers to the process involving the decomposition of intracellular components via lysosomes. Autophagy plays an important role in maintaining and regulating cell homeostasis by degrading intracellular components and providing degradation products to cells. In vivo, autophagy has been shown to be involved in the starvation response, intracellular quality control, early development, and cell differentiation. Recent studies have revealed that autophagy dysfunction is implicated in neurodegenerative diseases and tumorigenesis. In addition to the discovery of certain disease-causing autophagy-related mutations and elucidation of the pathogenesis of conditions resulting from the abnormal degradation of selective autophagy substrates, the activation of autophagy is essential for prolonging life and suppressing aging. This article provides a comprehensive review of the role of autophagy in health, physiological function, and autophagy-related disease. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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42 pages, 2996 KiB  
Review
Pathogenic Single Nucleotide Polymorphisms on Autophagy-Related Genes
by Isaac Tamargo-Gómez, Álvaro F. Fernández and Guillermo Mariño
Int. J. Mol. Sci. 2020, 21(21), 8196; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218196 - 02 Nov 2020
Cited by 14 | Viewed by 4112
Abstract
In recent years, the study of single nucleotide polymorphisms (SNPs) has gained increasing importance in biomedical research, as they can either be at the molecular origin of a determined disorder or directly affect the efficiency of a given treatment. In this regard, sequence [...] Read more.
In recent years, the study of single nucleotide polymorphisms (SNPs) has gained increasing importance in biomedical research, as they can either be at the molecular origin of a determined disorder or directly affect the efficiency of a given treatment. In this regard, sequence variations in genes involved in pro-survival cellular pathways are commonly associated with pathologies, as the alteration of these routes compromises cellular homeostasis. This is the case of autophagy, an evolutionarily conserved pathway that counteracts extracellular and intracellular stressors by mediating the turnover of cytosolic components through lysosomal degradation. Accordingly, autophagy dysregulation has been extensively described in a wide range of human pathologies, including cancer, neurodegeneration, or inflammatory alterations. Thus, it is not surprising that pathogenic gene variants in genes encoding crucial effectors of the autophagosome/lysosome axis are increasingly being identified. In this review, we present a comprehensive list of clinically relevant SNPs in autophagy-related genes, highlighting the scope and relevance of autophagy alterations in human disease. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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27 pages, 2012 KiB  
Review
Irisin and Autophagy: First Update
by Mirko Pesce, Patrizia Ballerini, Teresa Paolucci, Iris Puca, Mohammad Hosein Farzaei and Antonia Patruno
Int. J. Mol. Sci. 2020, 21(20), 7587; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207587 - 14 Oct 2020
Cited by 29 | Viewed by 4881
Abstract
Aging and sedentary life style are considered independent risk factors for many disorders. Under these conditions, accumulation of dysfunctional and damaged cellular proteins and organelles occurs, resulting in a cellular degeneration and cell death. Autophagy is a conserved recycling pathway responsible for the [...] Read more.
Aging and sedentary life style are considered independent risk factors for many disorders. Under these conditions, accumulation of dysfunctional and damaged cellular proteins and organelles occurs, resulting in a cellular degeneration and cell death. Autophagy is a conserved recycling pathway responsible for the degradation, then turnover of cellular proteins and organelles. This process is a part of the molecular underpinnings by which exercise promotes healthy aging and mitigate age-related pathologies. Irisin is a myokine released during physical activity and acts as a link between muscles and other tissues and organs. Its main beneficial function is the change of subcutaneous and visceral adipose tissue into brown adipose tissue, with a consequential increase in thermogenesis. Irisin modulates metabolic processes, acting on glucose homeostasis, reduces systemic inflammation, maintains the balance between resorption and bone formation, and regulates the functioning of the nervous system. Recently, some of its pleiotropic and favorable properties have been attributed to autophagy induction, posing irisin as an important regulator of autophagy by exercise. This review article proposes to bring together for the first time the “state of the art” knowledge regarding the effects of irisin and autophagy. Furthermore, treatments on relation between exercise/myokines and autophagy have been also achieved. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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23 pages, 2024 KiB  
Review
Roles of Specialized Pro-Resolving Lipid Mediators in Autophagy and Inflammation
by Antonio Recchiuti, Elisa Isopi, Mario Romano and Domenico Mattoscio
Int. J. Mol. Sci. 2020, 21(18), 6637; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186637 - 10 Sep 2020
Cited by 12 | Viewed by 4237
Abstract
Autophagy is a catabolic pathway that accounts for degradation and recycling of cellular components to extend cell survival under stress conditions. In addition to this prominent role, recent evidence indicates that autophagy is crucially involved in the regulation of the inflammatory response, a [...] Read more.
Autophagy is a catabolic pathway that accounts for degradation and recycling of cellular components to extend cell survival under stress conditions. In addition to this prominent role, recent evidence indicates that autophagy is crucially involved in the regulation of the inflammatory response, a tightly controlled process aimed at clearing the inflammatory stimulus and restoring tissue homeostasis. To be efficient and beneficial to the host, inflammation should be controlled by a resolution program, since uncontrolled inflammation is the underlying cause of many pathologies. Resolution of inflammation is an active process mediated by a variety of mediators, including the so-called specialized pro-resolving lipid mediators (SPMs), a family of endogenous lipid autacoids known to regulate leukocyte infiltration and activities, and counterbalance cytokine production. Recently, regulation of autophagic mechanisms by these mediators has emerged, uncovering unappreciated connections between inflammation resolution and autophagy. Here, we summarize mechanisms of autophagy and resolution, focusing on the contribution of autophagy in sustaining paradigmatic examples of chronic inflammatory disorders. Then, we discuss the evidence that SPMs can restore dysregulated autophagy, hypothesizing that resolution of inflammation could represent an innovative approach to modulate autophagy and its impact on the inflammatory response. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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13 pages, 848 KiB  
Review
Disruption of Placental Homeostasis Leads to Preeclampsia
by Akitoshi Nakashima, Tomoko Shima, Sayaka Tsuda, Aiko Aoki, Mihoko Kawaguchi, Satoshi Yoneda, Akemi Yamaki-Ushijima, Shi-Bin Cheng, Surendra Sharma and Shigeru Saito
Int. J. Mol. Sci. 2020, 21(9), 3298; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21093298 - 07 May 2020
Cited by 13 | Viewed by 3645
Abstract
Placental homeostasis is directly linked to fetal well-being and normal fetal growth. Placentas are sensitive to various environmental stressors, including hypoxia, endoplasmic reticulum stress, and oxidative stress. Once placental homeostasis is disrupted, the placenta may rebel against the mother and fetus. Autophagy is [...] Read more.
Placental homeostasis is directly linked to fetal well-being and normal fetal growth. Placentas are sensitive to various environmental stressors, including hypoxia, endoplasmic reticulum stress, and oxidative stress. Once placental homeostasis is disrupted, the placenta may rebel against the mother and fetus. Autophagy is an evolutionally conservative mechanism for the maintenance of cellular and organic homeostasis. Evidence suggests that autophagy plays a crucial role throughout pregnancy, including fertilization, placentation, and delivery in human and mouse models. This study reviews the available literature discussing the role of autophagy in preeclampsia. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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27 pages, 1970 KiB  
Review
Roles of Autophagy in Oxidative Stress
by Hyeong Rok Yun, Yong Hwa Jo, Jieun Kim, Yoonhwa Shin, Sung Soo Kim and Tae Gyu Choi
Int. J. Mol. Sci. 2020, 21(9), 3289; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21093289 - 06 May 2020
Cited by 185 | Viewed by 9338
Abstract
Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator [...] Read more.
Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator has been clarified and expanded in the pathological response to redox signalling. Autophagy is a major sensor of the redox signalling. Reactive oxygen species (ROS) are highly reactive molecules that are generated as by-products of cellular metabolism, principally by mitochondria. Mitochondrial ROS (mROS) are beneficial or detrimental to cells depending on their concentration and location. mROS function as redox messengers in intracellular signalling at physiologically low level, whereas excessive production of mROS causes oxidative damage to cellular constituents and thus incurs cell death. Hence, the balance of autophagy-related stress adaptation and cell death is important to comprehend redox signalling-related pathogenesis. In this review, we attempt to provide an overview the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathology. Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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Addendum
Addendum: Pesce et al. Irisin and Autophagy: First Update. Int. J. Mol. Sci. 2020, 21, 7587
by Mirko Pesce, Patrizia Ballerini, Teresa Paolucci, Iris Puca, Mohammad Hosein Farzaei and Antonia Patruno
Int. J. Mol. Sci. 2021, 22(10), 5117; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105117 - 12 May 2021
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Abstract
We did not receive the copyright for Figure 2 in our published paper [...] Full article
(This article belongs to the Special Issue Autophagy in Health, Ageing and Disease 2.0)
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