Apoptosis and Autophagy

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: closed (9 December 2022) | Viewed by 19841

Special Issue Editor


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Guest Editor
Department of Visceral Thoracic and Vascular Surgery, Philipps University Marburg, Baldingerstrasse, 35043 Marburg, Germany
Interests: apoptosis; autophagy; cell death; solid cancer; thyroid cancer; neuro-endocrine neoplasia; epigenetics; gastrointestinal cancer
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Special Issue Information

Dear Colleagues,

Apoptosis and autophagy represent two fundamental cellular processes. They are involved in cell fate decision and they crosstalk each other through the involvement of different key players. Nonetheless, the ability of apoptosis to cause cell death is counterbalanced by its ability to inhibit the cell death mediated by autophagy. Autophagy can also inhibit apoptosis and cause cell death. The intimate crosstalk between apoptosis and autophagy is not definitely dissected yet. It can occur during embryogenesis, tissue development, cell maturation and senescence. Alterations of such intriguing mechanisms can occur during tumorigenesis and other pathologies in mammals. Further evidence is urgently needed to clarify these fine-tuned cellular processes.    

This Special Issue of Life focuses on the recent advances in apoptosis and autophagy. We look forward to your submissions.

Dr. Pietro Di Fazio
Guest Editor

Manuscript Submission Information

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Keywords

  • crosstalk between apoptosis and autophagy
  • apoptosis/autophagy and tumorigenesis
  • impairment of cell death in cancer
  • targeting
  • natural compounds
  • epigenetics

Published Papers (6 papers)

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Research

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16 pages, 3095 KiB  
Article
Evidence for a Strong Relationship between the Cytotoxicity and Intracellular Location of β-Amyloid
by Md. Aminul Haque, Md. Selim Hossain, Tahmina Bilkis, Md. Imamul Islam and Il-Seon Park
Life 2022, 12(4), 577; https://doi.org/10.3390/life12040577 - 13 Apr 2022
Cited by 2 | Viewed by 1850
Abstract
β-Amyloid (Aβ) is a hallmark peptide of Alzheimer’s disease (AD). Herein, we explored the mechanism underlying the cytotoxicity of this peptide. Double treatment with oligomeric 42-amino-acid Aβ (Aβ42) species, which are more cytotoxic than other conformers such as monomers and fibrils, resulted in [...] Read more.
β-Amyloid (Aβ) is a hallmark peptide of Alzheimer’s disease (AD). Herein, we explored the mechanism underlying the cytotoxicity of this peptide. Double treatment with oligomeric 42-amino-acid Aβ (Aβ42) species, which are more cytotoxic than other conformers such as monomers and fibrils, resulted in increased cytotoxicity. Under this treatment condition, an increase in intracellular localization of the peptide was observed, which indicated that the peptide administered extracellularly entered the cells. The cell-permeable peptide TAT-tagged Aβ42 (tAβ42), which was newly prepared for the study and found to be highly cell-permeable and soluble, induced Aβ-specific lamin protein cleavage, caspase-3/7-like DEVDase activation, and high cytotoxicity (5–10-fold higher than that induced by the wild-type oligomeric preparations). Oligomeric species enrichment and double treatment were not necessary for enhancing the cytotoxicity and intracellular location of the fusion peptide. Taiwaniaflavone, an inhibitor of the cytotoxicity of wild-type Aβ42 and tAβ42, strongly blocked the internalization of the peptides into the cells. These data imply a strong relationship between the cytotoxicity and intracellular location of the Aβ peptide. Based on these results, we suggest that agents that can reduce the cell permeability of Aβ42 are potential AD therapeutics. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy)
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19 pages, 10740 KiB  
Article
Renal Apoptosis in the Mycotoxicology of Penicillium polonicum and Ochratoxin A in Rats
by Ana Miljkovic and Peter Mantle
Life 2022, 12(3), 352; https://doi.org/10.3390/life12030352 - 28 Feb 2022
Cited by 3 | Viewed by 1958
Abstract
Penicillium polonicum K. M. Zaleski, which is common on foodstuffs in Balkan regions that are notable for their history of endemic nephropathy, has been shown experimentally to cause a striking histopathological renal change in rats that are given feed contaminated by this fungus. [...] Read more.
Penicillium polonicum K. M. Zaleski, which is common on foodstuffs in Balkan regions that are notable for their history of endemic nephropathy, has been shown experimentally to cause a striking histopathological renal change in rats that are given feed contaminated by this fungus. The nephrotoxic agent(s) are only partially characterized. The principal change seen in the cortico-medullary region is karyocytomegaly, but apoptosis, identified with the ApopTag® methodology, is the first response to a dietary extract of P. polonicum-molded wheat after a few days of exposure. Chromatin debris migrates along the nephrons into the medulla, but whether the damaged epithelial fate is via autophagy is unclear. In intermittent exposure experiments, renal apoptosis was resolved with the cessation of exposure and was restored with renewed exposure. Apoptosis became less evident after 3 months of chronic exposure. In contrast, a relatively high dose of dietary ochratoxin A, a potent nephrocarcinogen in male rats after many months of dietary exposure, gave no evidence of apoptosis in asymptomatic weanlings over a few days of dietary exposure. This was attributed to a masking effect by concomitant marked histological disruption in renal tissue. However, in young adults, renal apoptosis was a primary outcome of dietary exposure to either the P. polonicum extract or to ochratoxin A, but the histopathological response to the former was less distorted. The apparent conflicted use in the literature of P. polonicum as a descriptor is highlighted. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy)
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16 pages, 3413 KiB  
Article
Melibiose Confers a Neuroprotection against Cerebral Ischemia/Reperfusion Injury by Ameliorating Autophagy Flux via Facilitation of TFEB Nuclear Translocation in Neurons
by Zhiyuan Wu, Yongjie Zhang, Yuyuan Liu, Xuemei Chen, Zhiwen Huang, Xiaoming Zhao, Hongyun He and Yihao Deng
Life 2021, 11(9), 948; https://doi.org/10.3390/life11090948 - 10 Sep 2021
Cited by 8 | Viewed by 2430
Abstract
Autophagic/lysosomal dysfunction is a critical pathogenesis of neuronal injury after ischemic stroke. Trehalose has been validated to restore the impaired autophagy flux by boosting transcription factor EB (TFEB) nuclear translocation, but orally administrated trehalose can be greatly digested by intestinal trehalase before entering [...] Read more.
Autophagic/lysosomal dysfunction is a critical pathogenesis of neuronal injury after ischemic stroke. Trehalose has been validated to restore the impaired autophagy flux by boosting transcription factor EB (TFEB) nuclear translocation, but orally administrated trehalose can be greatly digested by intestinal trehalase before entering into brain. Melibiose (MEL), an analogue of trehalose, may thoroughly exert its pharmacological effects through oral administration due to absence of intestinal melibiase. The present study was to investigate whether melibiose could also confer a neuroprotection by the similar pharmacological mechanism as trehalose did after ischemic stroke. The rats were pretreated with melibiose for 7 days before middle cerebral artery occlusion (MCAO) surgery. Twenty-four hours following MCAO/reperfusion, the cytoplasmic and nuclear TFEB, and the proteins in autophagic/lysosomal pathway at the penumbra were detected by western blot and immunofluorescence, respectively. Meanwhile, the neurological deficit, neuron survival, and infarct volume were assessed to evaluate the therapeutic outcomes. The results showed that the neurological injury was significantly mitigated in MCAO+MEL group, compared with that in MCAO group. Meanwhile, nuclear TFEB expression in neurons at the penumbra was significantly promoted by melibiose. Moreover, melibiose treatment markedly enhanced autophagy flux, as reflected by the reinforced lysosomal capacity and reduced autophagic substrates. Furthermore, the melibiose-elicited neuroprotection was prominently counteracted by lysosomal inhibitor Bafilomycin A1 (Baf-A1). Contrarily, reinforcement of lysosomal capacity with EN6 further improved the neurological performance upon melibiose treatment. Our data suggests that melibiose-augmented neuroprotection may be achieved by ameliorating autophagy flux via facilitation of TFEB nuclear translocation in neurons after ischemic stroke. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy)
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Review

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16 pages, 1267 KiB  
Review
Crosstalk between Glycogen-Selective Autophagy, Autophagy and Apoptosis as a Road towards Modifier Gene Discovery and New Therapeutic Strategies for Glycogen Storage Diseases
by Marina Andjelkovic, Anita Skakic, Milena Ugrin, Vesna Spasovski, Kristel Klaassen, Sonja Pavlovic and Maja Stojiljkovic
Life 2022, 12(9), 1396; https://doi.org/10.3390/life12091396 - 08 Sep 2022
Cited by 1 | Viewed by 2103
Abstract
Glycogen storage diseases (GSDs) are rare metabolic monogenic disorders characterized by an excessive accumulation of glycogen in the cell. However, monogenic disorders are not simple regarding genotype–phenotype correlation. Genes outside the major disease-causing locus could have modulatory effect on GSDs, and thus explain [...] Read more.
Glycogen storage diseases (GSDs) are rare metabolic monogenic disorders characterized by an excessive accumulation of glycogen in the cell. However, monogenic disorders are not simple regarding genotype–phenotype correlation. Genes outside the major disease-causing locus could have modulatory effect on GSDs, and thus explain the genotype–phenotype inconsistencies observed in these patients. Nowadays, when the sequencing of all clinically relevant genes, whole human exomes, and even whole human genomes is fast, easily available and affordable, we have a scientific obligation to holistically analyze data and draw smarter connections between genotype and phenotype. Recently, the importance of glycogen-selective autophagy for the pathophysiology of disorders of glycogen metabolism have been described. Therefore, in this manuscript, we review the potential role of genes involved in glycogen-selective autophagy as modifiers of GSDs. Given the small number of genes associated with glycogen-selective autophagy, we also include genes, transcription factors, and non-coding RNAs involved in autophagy. A cross-link with apoptosis is addressed. All these genes could be analyzed in GSD patients with unusual discrepancies between genotype and phenotype in order to discover genetic variants potentially modifying their phenotype. The discovery of modifier genes related to glycogen-selective autophagy and autophagy will start a new chapter in understanding of GSDs and enable the usage of autophagy-inducing drugs for the treatment of this group of rare-disease patients. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy)
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26 pages, 12418 KiB  
Review
BH3-Only Proteins Noxa and Puma Are Key Regulators of Induced Apoptosis
by Rabih Roufayel, Khaled Younes, Ahmed Al-Sabi and Nimer Murshid
Life 2022, 12(2), 256; https://doi.org/10.3390/life12020256 - 09 Feb 2022
Cited by 30 | Viewed by 6917
Abstract
Apoptosis is an evolutionarily conserved and tightly regulated cell death pathway. Physiological cell death is important for maintaining homeostasis and optimal biological conditions by continuous elimination of undesired or superfluous cells. The BH3-only pro-apoptotic members are strong inducers of apoptosis. The pro-apoptotic BH3-only [...] Read more.
Apoptosis is an evolutionarily conserved and tightly regulated cell death pathway. Physiological cell death is important for maintaining homeostasis and optimal biological conditions by continuous elimination of undesired or superfluous cells. The BH3-only pro-apoptotic members are strong inducers of apoptosis. The pro-apoptotic BH3-only protein Noxa activates multiple death pathways by inhibiting the anti-apoptotic Bcl-2 family protein, Mcl-1, and other protein members leading to Bax and Bak activation and MOMP. On the other hand, Puma is induced by p53-dependent and p53-independent apoptotic stimuli in several cancer cell lines. Moreover, this protein is involved in several physiological and pathological processes, such as immunity, cancer, and neurodegenerative diseases. Future heat shock research could disclose the effect of hyperthermia on both Noxa and BH3-only proteins. This suggests post-transcriptional mechanisms controlling the translation of both Puma and Noxa mRNA in heat-shocked cells. This study was also the chance to recapitulate the different reactional mechanisms investigated for caspases. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy)
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15 pages, 2203 KiB  
Review
Physiological Roles of Apoptotic Cell Clearance: Beyond Immune Functions
by Minjoo Han, Gyoungah Ryu, Seong-Ah Shin, Jangeun An, Huiji Kim, Daeho Park, Dae-Hee Lee and Chang Sup Lee
Life 2021, 11(11), 1141; https://doi.org/10.3390/life11111141 - 26 Oct 2021
Cited by 2 | Viewed by 3124
Abstract
The clearance of apoptotic cells is known to be a critical step in maintaining tissue and organism homeostasis. This process is rapidly/promptly mediated by recruited or resident phagocytes. Phagocytes that engulf apoptotic cells have been closely linked to the release of anti-inflammatory cytokines [...] Read more.
The clearance of apoptotic cells is known to be a critical step in maintaining tissue and organism homeostasis. This process is rapidly/promptly mediated by recruited or resident phagocytes. Phagocytes that engulf apoptotic cells have been closely linked to the release of anti-inflammatory cytokines to eliminate inflammatory responses. Defective clearance of apoptotic cells can cause severe inflammation and autoimmune responses due to secondary necrosis of apoptotic cells. Recently accumulated evidence indicates that apoptotic cells and their clearance have important physiological roles in addition to immune-related functions. Herein, we review the current understanding of the mechanisms and fundamental roles of apoptotic cell clearance and the beneficial roles of apoptotic cells in physiological processes such as differentiation and development. Full article
(This article belongs to the Special Issue Apoptosis and Autophagy)
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