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Cells
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Autophagy and Inflammation in Chronic Disease
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Autophagy and Inflammation in Chronic Disease

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

Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 12612

Special Issue Editors

Dr. Leopold Eckhart

E-Mail Website
Guest Editor
Skin Biology Laboratory, Department of Dermatology, Medical University of Vienna, Vienna, Austria
Interests: apoptosis; autophagy; skin; inflammation; evolutionary genetics
Dr. Supawadee Sukseree

E-Mail Website
Guest Editor
Center for Anatomy and Cell Biology, Division of Cell and Developmental Biology, Medical University of Vienna, Vienna, Austria
Interests: autophagy; inflammation; skin; aging; neuromuscular diseases

Special Issue Information

Dear Colleagues, 

Autophagy is a degradative process that controls metabolism, stress resistance and specific functions of mammalian cells. In immune defense, autophagy participates in the breakdown of pathogens, control of intracellular and intercellular inflammatory signaling, and antigen presentation. Aging and many chronic inflammatory diseases are associated with dysfunction of autophagy, suggesting that alterations of the rate of autophagy may be worthwhile targets of therapies for tissue-restricted and systemic inflammation. Studies in cultured cells and genetically modified animal models have revealed important molecular regulators and cellular processes. However, the mechanistic relationship between autophagy and onset or progression of inflammatory diseases have remained unknown.

The aim of this Special Issue is to publish new insights into roles of autophagy in chronic inflammatory diseases. The emphasis of the articles will be on cellular metabolism, intra- and intercellular signaling, cell growth, differentiation and senescence. Studies utilizing well defined mouse models of diseases, cells isolated from clinical samples, and combinations thereof are of particular interest. Manuscripts focusing on cellular processes in organ-specific or systemic inflammatory diseases are welcome. In particular, we invite reports on molecular mechanisms by which autophagy affects inflammation and on molecular effects of inflammation on autophagy in non-immune cells.

Both original research articles and reviews are welcome in this Special Issue.

We look forward to receiving your contributions.

Dr. Supawadee Sukseree
Dr. Leopold Eckhart
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
  • Atherosclerosis
  • Arthritis
  • Cardiovascular diseases
  • Cancer
  • Chronic skin diseases
  • Inflammation
  • Hepatitis
  • Obesity
  • Respiratory diseases

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Published Papers (4 papers)

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Research

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10 pages, 1102 KiB  
Article
Inactivation of Autophagy in Keratinocytes Reduces Tumor Growth in Mouse Models of Epithelial Skin Cancer
by Caterina Barresi, Heidemarie Rossiter, Maria Buchberger, Johannes Pammer, Supawadee Sukseree, Maria Sibilia, Erwin Tschachler and Leopold Eckhart
Cells 2022, 11(22), 3691; https://doi.org/10.3390/cells11223691 - 21 Nov 2022
Cited by 6 | Viewed by 1789
Abstract
Autophagy is a ubiquitous degradation mechanism, which plays a critical role in cellular homeostasis. To test whether autophagy suppresses or supports the growth of tumors in the epidermis of the skin, we inactivated the essential autophagy gene Atg7 specifically in the epidermal keratinocytes [...] Read more.
Autophagy is a ubiquitous degradation mechanism, which plays a critical role in cellular homeostasis. To test whether autophagy suppresses or supports the growth of tumors in the epidermis of the skin, we inactivated the essential autophagy gene Atg7 specifically in the epidermal keratinocytes of mice (Atg7∆ep) and subjected such mutant mice and fully autophagy-competent mice to tumorigenesis. The lack of epithelial Atg7 did not prevent tumor formation in response to 7, 12-dimethylbenz(a)anthracene (DMBA) as the initiator and 12-O tetradecanoylphorbol-13-acetate (TPA) as the promoter of tumor growth. However, the number of tumors per mouse was reduced in mice with epithelial Atg7 deficiency. In the K5-SOS EGFRwa2/wa2 mouse model, epithelial tumors were initiated by Son of sevenless (SOS) in response to wounding. Within 12 weeks after tumor initiation, 60% of the autophagy-competent K5-SOS EGFRwa2/wa2 mice had tumors of 1 cm diameter and had to be sacrificed, whereas none of the Atg7∆ep K5-SOS EGFRwa2/wa2 mice formed tumors of this size. In summary, the deletion of Atg7 reduced the growth of epithelial tumors in these two mouse models of skin cancer. Thus, our data show that the inhibition of autophagy limits the growth of epithelial skin tumors. Full article
(This article belongs to the Special Issue Autophagy and Inflammation in Chronic Disease)
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16 pages, 7266 KiB  
Article
Effects of Elamipretide on Autophagy in Renal Cells of Pigs with Metabolic Syndrome
by Siting Hong, Ramyar Ghandriz, Sarosh Siddiqi, Xiang-Yang Zhu, Ishran M. Saadiq, Kyra L. Jordan, Hui Tang, Khaled A. Ali, Amir Lerman, Alfonso Eirin and Lilach O. Lerman
Cells 2022, 11(18), 2891; https://doi.org/10.3390/cells11182891 - 16 Sep 2022
Cited by 1 | Viewed by 2890
Abstract
Autophagy eliminates excessive nutrients and maintains homeostasis. Obesity and metabolic syndrome (MetS) dysregulate autophagy, possibly partly due to mitochondria injury and inflammation. Elamipretide (ELAM) improves mitochondrial function. We hypothesized that MetS blunts kidney autophagy, which ELAM would restore. Domestic pigs were fed a [...] Read more.
Autophagy eliminates excessive nutrients and maintains homeostasis. Obesity and metabolic syndrome (MetS) dysregulate autophagy, possibly partly due to mitochondria injury and inflammation. Elamipretide (ELAM) improves mitochondrial function. We hypothesized that MetS blunts kidney autophagy, which ELAM would restore. Domestic pigs were fed a control or MetS-inducing diet for 16 weeks. During the 4 last weeks, MetS pigs received subcutaneous injections of ELAM (0.1 mg/kg/day, MetS + ELAM) or vehicle (MetS), and kidneys were then harvested to measure protein expression of autophagy mediators and apoptosis. Systemic and renal venous levels of inflammatory cytokines were measured to calculate renal release. The function of isolated mitochondria was assessed by oxidative stress, energy production, and pro-apoptotic activity. MetS slightly downregulated renal expression of autophagy mediators including p62, ATG5-12, mTOR, and AMPK vs. control. Increased mitochondrial H2O2 production accompanied decreased ATP production, elevated apoptosis, and renal fibrosis. In MetS + ELAM, mito-protection restored autophagic protein expression, improved mitochondrial energetics, and blunted renal cytokine release and fibrosis. In vitro, mitoprotection restored mitochondrial membrane potential and reduced oxidative stress in injured proximal tubular epithelial cells. Our study suggests that swine MetS mildly affects renal autophagy, possibly secondary to mitochondrial damage, and may contribute to kidney structural damage in MetS. Full article
(This article belongs to the Special Issue Autophagy and Inflammation in Chronic Disease)
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17 pages, 5182 KiB  
Article
Identification and Validation of Autophagy-Related Genes in Vitiligo
by Yiwen Yang, Xiuyi Wu, Xiaoli Lu, Chen Wang, Leihong Xiang and Chengfeng Zhang
Cells 2022, 11(7), 1116; https://doi.org/10.3390/cells11071116 - 25 Mar 2022
Cited by 10 | Viewed by 3561
Abstract
Vitiligo is a common depigmented disease with unclear pathogenesis. Autophagy is crucial for maintaining cellular homeostasis and has been linked to a variety of autoimmune disorders; however, there have been no reports exploring the involvement of autophagy-related genes (ARGs) in vitiligo using bioinformatics [...] Read more.
Vitiligo is a common depigmented disease with unclear pathogenesis. Autophagy is crucial for maintaining cellular homeostasis and has been linked to a variety of autoimmune disorders; however, there have been no reports exploring the involvement of autophagy-related genes (ARGs) in vitiligo using bioinformatics methodologies. In this study, RNA-sequencing technology was used to identify the differentially expressed genes (DEGs) and the Human Autophagy Database (HADb) was overlapped to identify differentially expressed autophagy-related genes (DEARGs) in stable non-segmental vitiligo (NSV). Bioinformatics analyses were conducted with R packages and Ingenuity Pathways Analysis (IPA). DEARGs were further confirmed with qRT-PCR. Critical autophagy markers were detected with Western blotting analysis. We identified a total of 39 DEARGs in vitiligo lesions. DEARGs-enriched canonical pathways, diseases and bio functions, upstream regulators, and networks were discovered. qRT-PCR confirmed the significant increases in FOS and RGS19 in vitiligo lesions. Lower microtubule-associated protein 1 light chain (LC3) II/LC3I ratio and higher sequestosome 1 (SQSTM1, p62) expression were found in vitiligo lesions. In conclusion, this study provided a new insight that autophagy dysregulation appeared in stable vitiligo lesions and might be involved in the etiology of vitiligo by taking part in multiple pathways and bio functions. Full article
(This article belongs to the Special Issue Autophagy and Inflammation in Chronic Disease)
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Review

Jump to: Research

37 pages, 1061 KiB  
Review
Targeting Autophagy Using Long Non-Coding RNAs (LncRNAs): New Landscapes in the Arena of Cancer Therapeutics
by Aviral Kumar, Sosmitha Girisa, Mohammed S. Alqahtani, Mohamed Abbas, Mangala Hegde, Gautam Sethi and Ajaikumar B. Kunnumakkara
Cells 2023, 12(5), 810; https://doi.org/10.3390/cells12050810 - 6 Mar 2023
Cited by 14 | Viewed by 3389
Abstract
Cancer has become a global health hazard accounting for 10 million deaths in the year 2020. Although different treatment approaches have increased patient overall survival, treatment for advanced stages still suffers from poor clinical outcomes. The ever-increasing prevalence of cancer has led to [...] Read more.
Cancer has become a global health hazard accounting for 10 million deaths in the year 2020. Although different treatment approaches have increased patient overall survival, treatment for advanced stages still suffers from poor clinical outcomes. The ever-increasing prevalence of cancer has led to a reanalysis of cellular and molecular events in the hope to identify and develop a cure for this multigenic disease. Autophagy, an evolutionary conserved catabolic process, eliminates protein aggregates and damaged organelles to maintain cellular homeostasis. Accumulating evidence has implicated the deregulation of autophagic pathways to be associated with various hallmarks of cancer. Autophagy exhibits both tumor-promoting and suppressive effects based on the tumor stage and grades. Majorly, it maintains the cancer microenvironment homeostasis by promoting viability and nutrient recycling under hypoxic and nutrient-deprived conditions. Recent investigations have discovered long non-coding RNAs (lncRNAs) as master regulators of autophagic gene expression. lncRNAs, by sequestering autophagy-related microRNAs, have been known to modulate various hallmarks of cancer, such as survival, proliferation, EMT, migration, invasion, angiogenesis, and metastasis. This review delineates the mechanistic role of various lncRNAs involved in modulating autophagy and their related proteins in different cancers. Full article
(This article belongs to the Special Issue Autophagy and Inflammation in Chronic Disease)
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