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Diseases
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Selective Autophagy in Aging and Disease
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Selective Autophagy in Aging and Disease

A special issue of Diseases (ISSN 2079-9721).

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 7133

Special Issue Editor

Dr. Alessandra Stacchiotti

E-Mail Website1 Website2
Guest Editor
1. Department of Biomedical Sciences for Health, University of Milan, Via Mangiagalli 31, 20133 Milan, Italy
2. UO Laboratorio di Morfologia Umana Applicata, IRCCS San Donato, 20133 Milan, Italy
Interests: translational preclinical models of diseases; metabolic diseases; oxidative damage; endoplasmic reticulum stress; mitochondria; autophagy; mitophagy; role of antioxidants; ageing; sirtuins; natural compounds to limit metabolic diseases; cardiovascular damage and sirtuins modulation; obesity and mitochondrial endoplasmic reticulum interplay; selective autophagy in aging and disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

“Recycling and dismantling” are fundamental words to keep our environment clean but they are also suitable for the inner cellular environment involving autophagy. In past years, more research has been performed on a specific or random autophagy (called macroautophagy or chaperone-mediated autophagy). Currently, the definitive digestion of excessive dismantled materials, dysfunctional organelles, or pathogens (bacteria and virus) is analyzed via a specific cargo-recognition mechanism called “selective autophagy”. Selective autophagy is largely conserved from yeast to human cells and is rapidly emerging as a crucial mechanism to maintain homeostasis and well-being. Thus, aberrant selective autophagy, if excessive or reduced, may occur in human inflammatory, degenerative or metabolic diseases and cancer. This Special Issue aims to exchange ideas in the field, to collect original research and review articles, and to extend the knowledge of extraordinary cellular signaling and its regulation from bench to bedside.

As such, your indispensable scientific contributions on new stimulating resources in the fascinating field of autophagy are eagerly awaited.

Dr. Alessandra Stacchiotti
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. Diseases is an international peer-reviewed open access monthly 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 1800 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

  • Mitophagy
  • Pexophagy
  • Xenophagy
  • ER-phagy
  • Cardiovascular diseases
  • Metabolic diseases
  • Neurodegenerative diseases
  • Cancer
  • COVID-19

Published Papers (2 papers)

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Research

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18 pages, 3281 KiB  
Article
Potential Combination Drug Therapy to Prevent Redox Stress and Mitophagy Dysregulation in Retinal Müller Cells under High Glucose Conditions: Implications for Diabetic Retinopathy
by Lalit Pukhrambam Singh and Takhellambam S. Devi
Diseases 2021, 9(4), 91; https://doi.org/10.3390/diseases9040091 - 14 Dec 2021
Cited by 8 | Viewed by 3377
Abstract
Chronic hyperglycemia-induced thioredoxin-interacting protein (TXNIP) expression, associated oxidative/nitrosative stress (ROS/RNS), and mitochondrial dysfunction play critical roles in the etiology of diabetic retinopathy (DR). However, there is no effective drug treatment to prevent or slow down the progression of DR. The purpose of this [...] Read more.
Chronic hyperglycemia-induced thioredoxin-interacting protein (TXNIP) expression, associated oxidative/nitrosative stress (ROS/RNS), and mitochondrial dysfunction play critical roles in the etiology of diabetic retinopathy (DR). However, there is no effective drug treatment to prevent or slow down the progression of DR. The purpose of this study is to examine if a combination drug treatment targeting TXNIP and the mitochondria-lysosome pathway prevents high glucose-induced mitochondrial stress and mitophagic flux in retinal Müller glial cells in culture, relevant to DR. We show that diabetes induces TXNIP expression, redox stress, and Müller glia activation (gliosis) in rat retinas when compared to non-diabetic rat retinas. Furthermore, high glucose (HG, 25 mM versus low glucose, LG 5.5 mM) also induces TXNIP expression and mitochondrial stress in a rat retinal Müller cell line, rMC1, in in vitro cultures. Additionally, we develop a mitochondria-targeted mCherry and EGFP probe tagged with two tandem COX8a mitochondrial target sequences (adenovirus-CMV-2×mt8a-CG) to examine mitophagic flux in rMC1. A triple drug combination treatment was applied using TXNIP-IN1 (which inhibits TXNIP interaction with thioredoxin), Mito-Tempo (mitochondrial anti-oxidant), and ML-SA1 (lysosome targeted activator of transient calcium channel MCOLN1/TRPML1 and of transcription factor TFEB) to study the mitochondrial–lysosomal axis dysregulation. We found that HG induces TXNIP expression, redox stress, and mitophagic flux in rMC1 versus LG. Treatment with the triple drug combination prevents mitophagic flux and restores transcription factor TFEB and PGC1α nuclear localization under HG, which is critical for lysosome biosynthesis and mitogenesis, respectively. Our results demonstrate that 2×mt8a-CG is a suitable probe for monitoring mitophagic flux, both in live and fixed cells in in vitro experiments, which may also be applicable to in vivo animal studies, and that the triple drug combination treatment has the potential for preventing retinal injury and disease progression in diabetes. Full article
(This article belongs to the Special Issue Selective Autophagy in Aging and Disease)
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Review

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12 pages, 761 KiB  
Review
Potential Diets to Improve Mitochondrial Activity in Amyotrophic Lateral Sclerosis
by Sayuri Yoshikawa, Kurumi Taniguchi, Haruka Sawamura, Yuka Ikeda, Ai Tsuji and Satoru Matsuda
Diseases 2022, 10(4), 117; https://doi.org/10.3390/diseases10040117 - 1 Dec 2022
Cited by 3 | Viewed by 3115
Abstract
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease, the pathogenesis of which is based on alternations in the mitochondria of motor neurons, causing their progressive death. A growing body of evidence shows that more efficient mitophagy could prevent and/or treat this disorder [...] Read more.
Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease, the pathogenesis of which is based on alternations in the mitochondria of motor neurons, causing their progressive death. A growing body of evidence shows that more efficient mitophagy could prevent and/or treat this disorder by suppressing mitochondrial dysfunction-induced oxidative stress and inflammation. Mitophagy has been considered one of the main mechanisms responsible for mitochondrial quality control. Since ALS is characterized by enormous oxidative stress, several edible phytochemicals that can activate mitophagy to remove damaged mitochondria could be considered a promising option to treat ALS by providing neuroprotection. Therefore, it is of great significance to explore the mechanisms of mitophagy in ALS and to understand the effects and/or molecular mechanisms of phytochemical action, which could translate into a treatment for neurodegenerative diseases, including ALS. Full article
(This article belongs to the Special Issue Selective Autophagy in Aging and Disease)
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