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Autophagy in Cell Survival and Death

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

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 35085

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Special Issue Editor

Dr. Deok Ryong Kim

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Guest Editor

Department of Biochemistry, College of Medicine and Institute of Health Sciences, Gyeongsang National University, JinJu 660-751, Republic of Korea
Interests: autophagy; cancer progression; adipogenesis; gene expression; systems biology

Special Issue Information

Dear Colleague

This Special Issue aims to cover various facets of the mechanism and regulation of autophagy in cell survival and death. It also includes the role of autophagy in many cellular processes and disease manifestations, such as responses to stressors, inflammatory responses, cancer progression, adipogenesis and neurodegeneration. In addition, systematic and comprehensive autophagy analyses using various publicly accessible datasets (RNA-seq, ChIP-seq, or others) in cellular processes or disease manifestations will be acceptable contributions. We welcome authors to submit original research papers or up-to-date review articles to this thematic issue.

This Special Issue will be comprehensive in relation to the general mechanisms of autophagy, drug-targeted regulation of autophagy, and autophagy regulators using new therapeutic strategies.

Dr. Deok Ryong Kim
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

autophagy regulation
autophagy-related genes
cell development and differentiation
cell survival and death
cancer progression
gene expression and regulation

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Published Papers (11 papers)

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Editorial

Jump to: Research, Review

4 pages, 573 KiB

Open AccessEditorial

Autophagy in Cell Survival and Death

by Jinsung Yang, Wanil Kim and Deok Ryong Kim

Int. J. Mol. Sci. 2023, 24(5), 4744; https://doi.org/10.3390/ijms24054744 - 1 Mar 2023

Cited by 6 | Viewed by 2466

Abstract

Autophagy is a degradative process to remove damaged or unnecessary cellular components, and it has been implicated in many biological processes during cell survival and death [...] Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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Research

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21 pages, 8966 KiB

Open AccessArticle

Spermidine-Eugenol Supplement Preserved Inflammation-Challenged Intestinal Cells by Stimulating Autophagy

by Francesca Truzzi, Anne Whittaker, Eros D’Amen, Maria Chiara Valerii, Veronika Abduazizova, Enzo Spisni and Giovanni Dinelli

Int. J. Mol. Sci. 2023, 24(4), 4131; https://doi.org/10.3390/ijms24044131 - 18 Feb 2023

Cited by 8 | Viewed by 4116

Abstract

Increases in non-communicable and auto-immune diseases, with a shared etiology of defective autophagy and chronic inflammation, have motivated research both on natural products in drug discovery fields and on the interrelationship between autophagy and inflammation. Within this framework, the tolerability and protective effects of a wheat-germ spermidine (SPD) and clove eugenol (EUG) combination supplement (SUPPL) were investigated on inflammation status (after the administration of lipopolysaccharide (LPS)) and on autophagy using human Caco-2 and NCM460 cell lines. In comparison to the LPS treatment alone, the SUPPL + LPS significantly attenuated ROS levels and midkine expression in monocultures, as well as occludin expression and mucus production in reconstituted intestinal equivalents. Over a timeline of 2–4 h, the SUPPL and SUPPL + LPS treatments stimulated autophagy LC3-11 steady state expression and turnover, as well as P62 turnover. After completely blocking autophagy with dorsomorphin, inflammatory midkine was significantly reduced in the SUPPL + LPS treatment in a non-autophagy-dependent manner. After a 24 h timeline, preliminary results showed that mitophagy receptor BNIP3L expression was significantly downregulated in the SUPPL + LPS treatment compared to the LPS alone, whereas conventional autophagy protein expression was significantly higher. The SUPPL shows promise in reducing inflammation and increasing autophagy to improve intestinal health. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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10 pages, 2138 KiB

Open AccessArticle

Chrysin Induces Apoptosis via the MAPK Pathway and Regulates ERK/mTOR-Mediated Autophagy in MC-3 Cells

by Gi-Hwan Jung, Jae-Han Lee, So-Hee Han, Joong-Seok Woo, Eun-Young Choi, Su-Ji Jeon, Eun-Ji Han, Soo-Hyun Jung, Young-Seok Park, Byung-Kwon Park, Byeong-Soo Kim, Sang-Ki Kim and Ji-Youn Jung

Int. J. Mol. Sci. 2022, 23(24), 15747; https://doi.org/10.3390/ijms232415747 - 12 Dec 2022

Cited by 10 | Viewed by 2852

Abstract

Chrysin is a flavonoid found abundantly in substances, such as honey and phytochemicals, and is known to exhibit anticancer effects against various cancer cells. Nevertheless, the anticancer effect of chrysin against oral cancer has not yet been verified. Furthermore, the mechanism underlying autophagy is yet to be clearly elucidated. Thus, this study investigated chrysin-mediated apoptosis and autophagy in human mucoepidermoid carcinoma (MC-3) cells. The change in MC-3 cell viability was examined using a 3-(4,5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide cell viability assay, as well as 40,6-diamidino-2-phenylindole, annexin V, and propidium iodide staining. Western blotting was used to analyze the proteins related to apoptosis and the mitogen-activated protein kinase (MAPK) pathway. In addition, the presence or absence of autophagy and changes in the expression of related proteins were investigated using acridine orange staining and Western blot. The results suggested that chrysin induced apoptosis and autophagy in MC-3 oral cancer cells via the MAPK/extracellular signal-regulated kinase pathway. Moreover, the induced autophagy exerted a cytoprotective effect against apoptosis. Thus, the further reduced cell viability due to autophagy as well as apoptosis induction highlight therapeutic potential of chrysin for oral cancer. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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18 pages, 5410 KiB

Open AccessArticle

Restoration of Cathepsin D Level via L-Serine Attenuates PPA-Induced Lysosomal Dysfunction in Neuronal Cells

by Hyunbum Jeon, Yeo Jin Kim, Su-Kyeong Hwang, Jinsoo Seo and Ji Young Mun

Int. J. Mol. Sci. 2022, 23(18), 10613; https://doi.org/10.3390/ijms231810613 - 13 Sep 2022

Cited by 6 | Viewed by 2833

Abstract

L-serine is a non-essential amino acid endogenously produced by astrocytes and is abundant in human diets. Beneficial roles of the metabolic products from L-serine in various conditions in the brain including neuronal development have been reported. Through several preclinical studies, L-serine treatment was also shown to offer beneficial therapeutic effects for brain damage such as ischemic stroke, amyotrophic lateral sclerosis, and Parkinson’s disease. Despite evidence for the value of L-serine in the clinic, however, its beneficial effects on the propionic acid (PPA)-induced neuronal toxicity and underlying mechanisms of L-serine-mediated neuroprotection are unknown. In this study, we observed that PPA-induced acidic stress induces abnormal lipid accumulation and functional defects in lysosomes of hippocampal neurons. L-serine treatment was able to rescue the structure and function of lysosomes in PPA-treated hippocampal neuronal cells. We further identified that L-serine suppressed the formation of lipid droplets and abnormal lipid membrane accumulations inside the lysosomes in PPA-treated hippocampal neuronal cells. Taken together, these findings indicate that L-serine can be utilized as a neuroprotective agent for the functionality of lysosomes through restoration of cathepsin D in disease conditions. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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9 pages, 1235 KiB

Open AccessArticle

Zinc Deficiency Induces Autophagy in HT-22 Mouse Hippocampal Neuronal Cell Line

by Si-Yeon Kim, Jung-Ho Lee and Soon-Ae Kim

Int. J. Mol. Sci. 2022, 23(15), 8811; https://doi.org/10.3390/ijms23158811 - 8 Aug 2022

Cited by 7 | Viewed by 2680

Abstract

Zinc is a trace metal vital for various functions in nerve cells, although the effect of zinc deficiency on neuronal autophagy remains unclear. This study aimed to elucidate whether zinc deficiency induced by treatment with N, N, N′, N′-tetrakis (2-pyridylmethyl) ethylenediamine (TPEN), a zinc chelator, affects and alters autophagy activity. In cell viability assays, TPEN showed cytotoxicity in HT-22 cells. TPEN treatment also increased LC3-II levels and the ratio of LC3-II to LC3-I. Western blot analysis showed that phospho-AMP-activated protein kinase levels and the ratio of phospho-AMP-activated protein kinase to total AMP-activated protein kinase increased. Protein levels of the mammalian target of rapamycin and sirtuin 1 decreased following TPEN treatment. When TPEN-treated HT-22 cells were cotreated with autophagy inhibitors, 3-methyladenine (1 mM), or bafilomycin A1 (3 nM), the TPEN-induced decrease in cell viability was exacerbated. Cotreatment with chloroquine (10 μM) partially restored cell viability. The study showed that zinc deficiency induces autophagy and may be cytoprotective in neurons. We expect our results to add a new perspective to our understanding of the neuronal pathology related to zinc deficiency. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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14 pages, 3430 KiB

Open AccessArticle

Allethrin Promotes Apoptosis and Autophagy Associated with the Oxidative Stress-Related PI3K/AKT/mTOR Signaling Pathway in Developing Rat Ovaries

by Maroua Jalouli, Afoua Mofti, Yasser A. Elnakady, Saber Nahdi, Anouar Feriani, Abdelkarem Alrezaki, Khaled Sebei, Mariano Bizzarri, Saleh Alwasel and Abdel Halim Harrath

Int. J. Mol. Sci. 2022, 23(12), 6397; https://doi.org/10.3390/ijms23126397 - 7 Jun 2022

Cited by 29 | Viewed by 3307

Abstract

The increased concern regarding the reduction in female fertility and the impressive numbers of women undergoing fertility treatment support the existence of environmental factors beyond inappropriate programming of developing ovaries. Among these factors are pyrethroids, which are currently some of the most commonly used pesticides worldwide. The present study was performed to investigate the developmental effects of the pyrethroid-based insecticide allethrin on ovarian function in rat offspring in adulthood. We mainly focused on the roles of oxidative stress, apoptosis, autophagy and the related pathways in ovarian injury. Thirty-day-old Wistar albino female rats were intragastrically administered 0 (control), 34.2 or 68.5 mg/kg body weight allethrin after breeding from Day 6 of pregnancy until delivery. We found that allethrin-induced ovarian histopathological damage was accompanied by elevations in oxidative stress and apoptosis. Interestingly, the number of autophagosomes in allethrin-treated ovaries was higher, and this increase was correlated with the upregulated expression of genes and proteins related to the autophagic marker LC-3. Furthermore, allethrin downregulated the expression of PI3K, AKT and mTOR in allethrin-treated ovaries compared with control ovaries. Taken together, the findings of this study suggest that exposure to the pyrethroid-based insecticide allethrin adversely affects both the follicle structure and function in rat offspring during adulthood. Specifically, allethrin can induce excessive oxidative stress and defective autophagy-related apoptosis, probably through inactivation of the PI3K/AKT/mTOR signaling pathway, and these effects may contribute to ovarian dysfunction and impaired fertility in female offspring. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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13 pages, 4150 KiB

Open AccessArticle

Fatty Acid Binding Protein 6 Inhibition Decreases Cell Cycle Progression, Migration and Autophagy in Bladder Cancers

by Chieh-Hsin Lin, Hsin-Han Chang, Chien-Rui Lai, Hisao-Hsien Wang, Wen-Chiuan Tsai, Yu-Ling Tsai, Chih-Ying Changchien, Yu-Chen Cheng, Sheng-Tang Wu and Ying Chen

Int. J. Mol. Sci. 2022, 23(4), 2154; https://doi.org/10.3390/ijms23042154 - 15 Feb 2022

Cited by 19 | Viewed by 3718

Abstract

Bladder cancer (BC) has a high recurrence rate worldwide. The aim of this study was to evaluate the role of fatty acid binding protein 6 (FABP6) in proliferation and migration in human bladder cancer cells. Cell growth was confirmed by MTT and colony formation assay. Western blotting was used to explore protein expressions. Wound healing and Transwell assays were performed to evaluate the migration ability. A xenograft animal model with subcutaneous implantation of BC cells was generated to confirm the tumor progression. Knockdown of FABP6 reduced cell growth in low-grade TSGH-8301 and high-grade T24 cells. Cell cycle blockade was observed with the decrease of CDK2, CDK4, and Ki67 levels in FABP6-knockdown BC cells. Interestingly, knockdown of FBAP6 led to downregulation of autophagic markers and activation of AKT-mTOR signaling. The application of PI3K/AKT inhibitor decreased cell viability mediated by FABP6-knockdown additionally. Moreover, FABP6-knockdown reduced peroxisome proliferator-activated receptor γ and retinoid X receptor α levels but increased p-p65 expression. Knockdown of FABP6 also inhibited BC cell motility with focal adhesive complex reduction. Finally, shFABP6 combined with cisplatin suppressed tumor growth in vivo. These results provide evidence that FABP6 may be a potential target in BC cells progression. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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26 pages, 14169 KiB

Open AccessArticle

The Autophagy-Related Organelle Autophagoproteasome Is Suppressed within Ischemic Penumbra

by Francesca Biagioni, Federica Mastroiacovo, Paola Lenzi, Stefano Puglisi-Allegra, Carla L. Busceti, Larisa Ryskalin, Rosangela Ferese, Domenico Bucci, Alessandro Frati, Ferdinando Nicoletti and Francesco Fornai

Int. J. Mol. Sci. 2021, 22(19), 10364; https://doi.org/10.3390/ijms221910364 - 26 Sep 2021

Cited by 7 | Viewed by 2306

Abstract

The peri-infarct region, which surrounds the irreversible ischemic stroke area is named ischemic penumbra. This term emphasizes the borderline conditions for neurons placed within such a critical region. Area penumbra separates the ischemic core, where frank cell loss occurs, from the surrounding healthy brain tissue. Within such a brain region, nervous matter, and mostly neurons are impaired concerning metabolic conditions. The classic biochemical marker, which reliably marks area penumbra is the over-expression of the heat shock protein 70 (HSP70). However, other proteins related to cell clearing pathways are modified within area penumbra. Among these, autophagy proteins like LC3 increase in a way, which recapitulates Hsp70. In contrast, components, such as P20S, markedly decrease. Despite apparent discrepancies, the present study indicates remarkable overlapping between LC3 and P20S redistribution within area penumbra. In fact, the amount of both proteins is markedly reduced within vacuoles. Specifically, a massive loss of LC3 + P20S immuno-positive vacuoles (autophagoproteasomes) is reported here. This represents the most relevant sub-cellular alteration here described in cell clearing pathways within area penumbra. The functional significance of these findings remains to be determined and it will take a novel experimental stream to decipher the fine-tuning of such a phenomenon. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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Review

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17 pages, 2905 KiB

Open AccessReview

The Role of Alternative Mitophagy in Heart Disease

by Jihoon Nah

Int. J. Mol. Sci. 2023, 24(7), 6362; https://doi.org/10.3390/ijms24076362 - 28 Mar 2023

Cited by 8 | Viewed by 3104

Abstract

Autophagy is essential for maintaining cellular homeostasis through bulk degradation of subcellular constituents, including misfolded proteins and dysfunctional organelles. It is generally governed by the proteins Atg5 and Atg7, which are critical regulators of the conventional autophagy pathway. However, recent studies have identified an alternative Atg5/Atg7-independent pathway, i.e., Ulk1- and Rab9-mediated alternative autophagy. More intensive studies have identified its essential role in stress-induced mitochondrial autophagy, also known as mitophagy. Alternative mitophagy plays pathophysiological roles in heart diseases such as myocardial ischemia and pressure overload. Here, this review discusses the established and emerging mechanisms of alternative autophagy/mitophagy that can be applied in therapeutic interventions for heart disorders. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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14 pages, 1219 KiB

Open AccessReview

Viruses Binding to Host Receptors Interacts with Autophagy

by Jinsung Yang

Int. J. Mol. Sci. 2023, 24(4), 3423; https://doi.org/10.3390/ijms24043423 - 8 Feb 2023

Cited by 6 | Viewed by 3111

Abstract

Viruses must cross the plasma membrane to infect cells, making them eager to overcome this barrier in order to replicate in hosts. They bind to cell surface receptors as the first step of initiating entry. Viruses can use several surface molecules that allow them to evade defense mechanisms. Various mechanisms are stimulated to defend against viruses upon their entry into cells. Autophagy, one of the defense systems, degrades cellular components to maintain homeostasis. The presence of viruses in the cytosol regulates autophagy; however, the mechanisms by which viral binding to receptors regulates autophagy have not yet been fully established. This review discusses recent findings on autophagy induced by interactions between viruses and receptors. It provides novel perspectives on the mechanism of autophagy as regulated by viruses. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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13 pages, 698 KiB

Open AccessReview

Exogenous Hydrogen Sulfide Plays an Important Role by Regulating Autophagy in Diabetic-Related Diseases

by Shuangyu Lv, Huiyang Liu and Honggang Wang

Int. J. Mol. Sci. 2021, 22(13), 6715; https://doi.org/10.3390/ijms22136715 - 23 Jun 2021

Cited by 25 | Viewed by 3235

Abstract

Autophagy is a vital cell mechanism which plays an important role in many physiological processes including clearing long-lived, accumulated and misfolded proteins, removing damaged organelles and regulating growth and aging. Autophagy also participates in a variety of biological functions, such as development, cell differentiation, resistance to pathogens and nutritional hunger. Recently, autophagy has been reported to be involved in diabetes, but the mechanism is not fully understood. Hydrogen sulfide (H₂S) is a colorless, water-soluble, flammable gas with the typical odor of rotten eggs, which has been known as a highly toxic gas for many years. However, it has been reported recently that H₂S, together with nitric oxide and carbon monoxide, is an important gas signal transduction molecule. H₂S has been reported to play a protective role in many diabetes-related diseases, but the mechanism is not fully clear. Recent studies indicate that H₂S plays an important role by regulating autophagy in many diseases including cancer, tissue fibrosis diseases and glycometabolic diseases; however, the related mechanism has not been fully studied. In this review, we summarize recent research on the role of H₂S in regulating autophagy in diabetic-related diseases to provide references for future related research. Full article

(This article belongs to the Special Issue Autophagy in Cell Survival and Death)

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