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The Role of Autophagy Processes in Human Diseases
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The Role of Autophagy Processes in Human Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 December 2022) | Viewed by 16744

Special Issue Editors

Dr. Shan-Ying Wu

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
Interests: autophagy; tumor biology; molecular biology; cell biology; cell signaling
Dr. Ying-Ray Lee

E-Mail Website
Guest Editor
Department of Microbiology and Immunology, Kaohsiung Medical University, Kaohsiung, Taiwan
Interests: virology; cancer biology; autophagy; infectious diseases; cell biology; signaling transduction
Dr. Lan Sheng-Hui

E-Mail Website
Guest Editor
Department of Life Sciences and Institute of Genome Sciences, National Yang Ming Chiao Tung University, Taipei, Taiwan
Interests: autophagy; cell biology; molecular biology; cancer biology; cell signaling

Special Issue Information

Dear Colleagues, 

Autophagy processes regulate the developmental biology and progression of various diseases. In cancer, autophagy plays a diverse role in the oncogenic or tumor-suppressive functions in the different stages of cancer progression. Autophagy also coordinates its functions in the balance of metabolic homeostasis and the development of diabetes. Furthermore, autophagy deficiency is associated with the development of Parkinson’s disease, which is a neurodegenerative disease. In the viral infection areas, some viral infections induce autophagic activity in the host cells to enhance viral replication and facilitate the viral life cycle. Moreover, accumulating reports demonstrate that autophagy is not only a degradation pathway for component recycling in the cell but also an unconventional secretion process for specific cargo releasing. Some cytosolic proteins lack the signal peptides for trafficking from the endoplasmic reticulum and are secreted by different unconventional processes. Secretory autophagy participates in one of the unconventional secretion pathways. All these reports support the idea that clarifying the molecular mechanism of autophagy to strengthen our scientific knowledge is important.

In this Special Issue, we welcome original research articles, reviews, and short communications that focus on the field of autophagy research and aim to explore the molecular regulation of autophagy in physiology and pathology. Research areas may include (but not limited to) the following: cancer, diabetes mellites, neurodegenerative diseases, metabolic diseases, infectious diseases, cell biology, immunity, and developmental biology. We are hoping that this special issue could shed some light on the molecular research of autophagy in various human diseases.

We look forward to receiving your contributions.

Dr. Shan-Ying Wu
Dr. Ying-Ray Lee
Dr. Lan Sheng-Hui
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
  • cancer
  • metabolic disease
  • cell signaling
  • molecular mechanisms
  • therapeutic strategy

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Published Papers (6 papers)

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Research

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17 pages, 3392 KiB  
Article
Piperlongumine Induces Cellular Apoptosis and Autophagy via the ROS/Akt Signaling Pathway in Human Follicular Thyroid Cancer Cells
by Tsung-Hsing Lin, Chin-Ho Kuo, Yi-Sheng Zhang, Pin-Tzu Chen, Shu-Hsin Chen, Yi-Zhen Li and Ying-Ray Lee
Int. J. Mol. Sci. 2023, 24(9), 8048; https://doi.org/10.3390/ijms24098048 - 28 Apr 2023
Cited by 3 | Viewed by 1727
Abstract
Thyroid cancer (TC) is the most common endocrine malignancy. Recently, the global incidence of TC has increased rapidly. Differentiated thyroid cancer includes papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC), which are the most common types of TC. Although PTCs and FTCs [...] Read more.
Thyroid cancer (TC) is the most common endocrine malignancy. Recently, the global incidence of TC has increased rapidly. Differentiated thyroid cancer includes papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC), which are the most common types of TC. Although PTCs and FTCs exert good prognoses and high survival rates, FTCs tend to be more aggressive than PTCs. There is an urgent need to improve patient outcomes by developing effective therapeutic agents for FTCs. Piperlongumine exerts anti-cancer effects in various human carcinomas, including human anaplastic TCs and PTCs. However, the anti-cancer effects of piperlongumine in FTCs and the underlying mechanisms are yet to be elucidated. Therefore, in the present study, we evaluated the effect of piperlongumine on cell proliferation, cell cycle, apoptosis, and autophagy in FTC cells with flowcytometry and Western blot. We observed that piperlongumine caused growth inhibition, cell cycle arrest, apoptosis induction, and autophagy elevation in FTC cells. Activities of reactive oxygen species and the downstream PI3K/Akt pathway were the underlying mechanisms involved in piperlongumine mediated anti-FTC effects. Advancements in our understanding of the effects of piperlongumine in FTC hold promise for the development of novel therapeutic strategies. Full article
(This article belongs to the Special Issue The Role of Autophagy Processes in Human Diseases)
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14 pages, 3438 KiB  
Communication
NEAT1 Confers Radioresistance to Hepatocellular Carcinoma Cells by Inducing PINK1/Parkin-Mediated Mitophagy
by Hiroyuki Tsuchiya, Ririko Shinonaga, Hiromi Sakaguchi, Yutaka Kitagawa, Kenji Yoshida and Goshi Shiota
Int. J. Mol. Sci. 2022, 23(22), 14397; https://doi.org/10.3390/ijms232214397 - 19 Nov 2022
Cited by 12 | Viewed by 2300
Abstract
A long noncoding RNA, nuclear paraspeckle assembly transcript 1 (NEAT1) variant 1 (NEAT1v1), confers radioresistance to hepatocellular carcinoma (HCC) cells by inducing autophagy via γ-aminobutyric acid A receptor-associated protein (GABARAP). Radiation induces oxidative stress to damage cellular components and organelles, but it remains [...] Read more.
A long noncoding RNA, nuclear paraspeckle assembly transcript 1 (NEAT1) variant 1 (NEAT1v1), confers radioresistance to hepatocellular carcinoma (HCC) cells by inducing autophagy via γ-aminobutyric acid A receptor-associated protein (GABARAP). Radiation induces oxidative stress to damage cellular components and organelles, but it remains unclear how NEAT1v1 protects HCC cells from radiation-induced oxidative stress via autophagy. To address this, we precisely investigated NEAT1v1-induced autophagy in irradiated HCC cell lines. X-ray irradiation significantly increased cellular and mitochondrial oxidative stress and mitochondrial DNA content in HCC cells while NEAT1v1 suppressed them. NEAT1v1 concomitantly induced the phosphatase and tensin homolog-induced kinase 1 (PINK1)/parkin-mediated mitophagy. Interestingly, parkin expression was constitutively upregulated in NEAT1v1-overexpressing HCC cells, leading to increased mitochondrial parkin levels. Superoxide dismutase 2 (SOD2) was also upregulated by NEAT1v1, and GABARAP or SOD2 knockdown in NEAT1v1-overexpressing cells increased mitochondrial oxidative stress and mitochondrial DNA content after irradiation. Moreover, it was suggested that SOD2 was involved in NEAT1v1-induced parkin expression, and that GABARAP promoted parkin degradation via mitophagy. This study highlights the unprecedented roles of NEAT1v1 in connecting radioresistance and mitophagy in HCC. Full article
(This article belongs to the Special Issue The Role of Autophagy Processes in Human Diseases)
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Review

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27 pages, 2545 KiB  
Review
The Complex Relationship between Hypoxia Signaling, Mitochondrial Dysfunction and Inflammation in Calcific Aortic Valve Disease: Insights from the Molecular Mechanisms to Therapeutic Approaches
by Esmaa Bouhamida, Giampaolo Morciano, Gaia Pedriali, Daniela Ramaccini, Elena Tremoli, Carlotta Giorgi, Paolo Pinton and Simone Patergnani
Int. J. Mol. Sci. 2023, 24(13), 11105; https://doi.org/10.3390/ijms241311105 - 5 Jul 2023
Cited by 4 | Viewed by 2398
Abstract
Calcific aortic valve stenosis (CAVS) is among the most common causes of cardiovascular mortality in an aging population worldwide. The pathomechanisms of CAVS are such a complex and multifactorial process that researchers are still making progress to understand its physiopathology as well as [...] Read more.
Calcific aortic valve stenosis (CAVS) is among the most common causes of cardiovascular mortality in an aging population worldwide. The pathomechanisms of CAVS are such a complex and multifactorial process that researchers are still making progress to understand its physiopathology as well as the complex players involved in CAVS pathogenesis. Currently, there is no successful and effective treatment to prevent or slow down the disease. Surgical and transcatheter valve replacement represents the only option available for treating CAVS. Insufficient oxygen availability (hypoxia) has a critical role in the pathogenesis of almost all CVDs. This process is orchestrated by the hallmark transcription factor, hypoxia-inducible factor 1 alpha subunit (HIF-1α), which plays a pivotal role in regulating various target hypoxic genes and metabolic adaptations. Recent studies have shown a great deal of interest in understanding the contribution of HIF-1α in the pathogenesis of CAVS. However, it is deeply intertwined with other major contributors, including sustained inflammation and mitochondrial impairments, which are attributed primarily to CAVS. The present review aims to cover the latest understanding of the complex interplay effect of hypoxia signaling pathways, mitochondrial dysfunction, and inflammation in CAVS. We propose further hypotheses and interconnections on the complexity of these impacts in a perspective of better understanding the pathophysiology. These interplays will be examined considering recent studies that shall help us better dissect the molecular mechanism to enable the design and development of potential future therapeutic approaches that can prevent or slow down CAVS processes. Full article
(This article belongs to the Special Issue The Role of Autophagy Processes in Human Diseases)
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19 pages, 1245 KiB  
Review
The Roles of Mitophagy and Autophagy in Ineffective Erythropoiesis in β-Thalassemia
by Pornthip Chaichompoo, Saovaros Svasti and Duncan R. Smith
Int. J. Mol. Sci. 2022, 23(18), 10811; https://doi.org/10.3390/ijms231810811 - 16 Sep 2022
Cited by 7 | Viewed by 2871
Abstract
β-Thalassemia is one of the most common genetically inherited disorders worldwide, and it is characterized by defective β-globin chain synthesis leading to reduced or absent β-globin chains. The excess α-globin chains are the key factor leading to the death of differentiating erythroblasts in [...] Read more.
β-Thalassemia is one of the most common genetically inherited disorders worldwide, and it is characterized by defective β-globin chain synthesis leading to reduced or absent β-globin chains. The excess α-globin chains are the key factor leading to the death of differentiating erythroblasts in a process termed ineffective erythropoiesis, leading to anemia and associated complications in patients. The mechanism of ineffective erythropoiesis in β-thalassemia is complex and not fully understood. Autophagy is primarily known as a cell recycling mechanism in which old or dysfunctional proteins and organelles are digested to allow recycling of constituent elements. In late stage, erythropoiesis autophagy is involved in the removal of mitochondria as part of terminal differentiation. Several studies have shown that autophagy is increased in earlier erythropoiesis in β-thalassemia erythroblasts, as compared to normal erythroblasts. This review summarizes what is known about the role of autophagy in β-thalassemia erythropoiesis and shows that modulation of autophagy and its interplay with apoptosis may provide a new therapeutic route in the treatment of β-thalassemia. Literature was searched and relevant articles were collected from databases, including PubMed, Scopus, Prospero, Clinicaltrials.gov, Google Scholar, and the Google search engine. Search terms included: β-thalassemia, ineffective erythropoiesis, autophagy, novel treatment, and drugs during the initial search. Relevant titles and abstracts were screened to choose relevant articles. Further, selected full-text articles were retrieved, and then, relevant cross-references were scanned to collect further information for the present review. Full article
(This article belongs to the Special Issue The Role of Autophagy Processes in Human Diseases)
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12 pages, 1005 KiB  
Review
The Role of Autophagy and Pyroptosis in Liver Disorders
by Huijie Zhao, Huiyang Liu, Yihan Yang and Honggang Wang
Int. J. Mol. Sci. 2022, 23(11), 6208; https://doi.org/10.3390/ijms23116208 - 1 Jun 2022
Cited by 23 | Viewed by 3624
Abstract
Pyroptosis is a programmed cell death caused by inflammasomes, which can detect cell cytosolic contamination or disturbance. In pyroptosis, caspase-1 or caspase-11/4/5 is activated, cleaving gasdermin D to separate its N-terminal pore-forming domain (PFD). The oligomerization of PFD forms macropores in the membrane, [...] Read more.
Pyroptosis is a programmed cell death caused by inflammasomes, which can detect cell cytosolic contamination or disturbance. In pyroptosis, caspase-1 or caspase-11/4/5 is activated, cleaving gasdermin D to separate its N-terminal pore-forming domain (PFD). The oligomerization of PFD forms macropores in the membrane, resulting in swelling and membrane rupture. According to the different mechanisms, pyroptosis can be divided into three types: canonical pathway-mediated pyroptosis, non-canonical pathway-mediated pyroptosis, and caspase-3-induced pyroptosis. Pyroptosis has been reported to play an important role in many tissues and organs, including the liver. Autophagy is a highly conserved process of the eukaryotic cell cycle. It plays an important role in cell survival and maintenance by degrading organelles, proteins and macromolecules in the cytoplasm. Therefore, the dysfunction of this process is involved in a variety of pathological processes. In recent years, autophagy and pyroptosis and their interactions have been proven to play an important role in various physiological and pathological processes, and have gradually attracted more and more attention to become a research hotspot. Therefore, this review summarized the role of autophagy and pyroptosis in liver disorders, and analyzed the related mechanism to provide a basis for future research. Full article
(This article belongs to the Special Issue The Role of Autophagy Processes in Human Diseases)
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35 pages, 2680 KiB  
Review
Nutraceuticals as Modulators of Autophagy: Relevance in Parkinson’s Disease
by Michał Rakowski, Szymon Porębski and Agnieszka Grzelak
Int. J. Mol. Sci. 2022, 23(7), 3625; https://doi.org/10.3390/ijms23073625 - 26 Mar 2022
Cited by 13 | Viewed by 3158
Abstract
Dietary supplements and nutraceuticals have entered the mainstream. Especially in the media, they are strongly advertised as safe and even recommended for certain diseases. Although they may support conventional therapy, sometimes these substances can have unexpected side effects. This review is particularly focused [...] Read more.
Dietary supplements and nutraceuticals have entered the mainstream. Especially in the media, they are strongly advertised as safe and even recommended for certain diseases. Although they may support conventional therapy, sometimes these substances can have unexpected side effects. This review is particularly focused on the modulation of autophagy by selected vitamins and nutraceuticals, and their relevance in the treatment of neurodegenerative diseases, especially Parkinson’s disease (PD). Autophagy is crucial in PD; thus, the induction of autophagy may alleviate the course of the disease by reducing the so-called Lewy bodies. Hence, we believe that those substances could be used in prevention and support of conventional therapy of neurodegenerative diseases. This review will shed some light on their ability to modulate the autophagy. Full article
(This article belongs to the Special Issue The Role of Autophagy Processes in Human Diseases)
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