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Special Issue "Autophagy in Health and Diseases"

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

Deadline for manuscript submissions: 31 August 2023 | Viewed by 2650

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Dr. Jiahong Lu

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Guest Editor

State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau SAR 999078, China
Interests: chemotherapy; autophagy and biogenesis; Alzheimer’s disease pathology; neurobiology; cell biology; pharmacology

Special Issue Information

Dear Colleagues,

Our understanding of molecular mechanisms of autophagy has greatly expanded in the past 20 years. In recent years, the main interests of the autophagy research field have gradually shifted from pure mechanistic studies to revealing the role of autophagy in various physiological and pathological conditions. By establishing the causative link between autophagy dysregulation and diseases, scientist have attempted to determine whether autophagy can be a therapeutic target against a series of diseases, including neurodegenerative diseases and cancers. Indeed, an increasing number of autophagy modulatory compounds have been identified and tested in different disease models, while dozens of clinical trials targeting autophagy inhibition through chloroquine or hydroxychloroquine for the treatment of multiple cancers are ongoing. However, challenges remain, such as poor selectivity of autophagy regulation in different tissues, and approaches to modulate autophagy in patients are limited.

This Special Issue aims to collect exciting progress in deciphering the roles of autophagy in physiological and diseases conditions. The accumulation of studies in this area may pave the way for the development of therapeutic intervention for multiple diseases by targeting autophagy.

Dr. Jiahong Lu
Guest Editor

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Keywords

autophagy
neurodegenerative disease
cancer
inflammatory diseases
autophagy modulators

Published Papers (3 papers)

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Open AccessArticle

Transcriptome Sequencing Reveals Autophagy Networks in Rat Livers during the Development of NAFLD and Identifies Autophagy Hub Genes

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Int. J. Mol. Sci. 2023, 24(7), 6437; https://doi.org/10.3390/ijms24076437 - 29 Mar 2023

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Abstract

(1) Autophagy is an important biological process in cells and is closely associated with the development and progression of non-alcoholic fatty liver disease (NAFLD). Therefore, this study aims to investigate the biological function of the autophagy hub genes, which could be used as a potential therapeutic target and diagnostic markers for NAFLD. (2) Male C57BL/6J mice were sacrificed after 16 and 38 weeks of a high-fat diet, serum biochemical indexes were detected, and liver lobules were collected for pathological observation and transcriptome sequencing. The R software was used to identify differentially expressed autophagy genes (DEGs) from the transcriptome sequencing data of mice fed with a normal diet for 38 weeks (ND38) and a high-fat diet for 38 weeks (HFD38). Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed on the DEGs, a protein–protein interaction (PPI) network of the DEGs was established using the STRING data website, and the results were visualized through Cytoscape. (3) After 16 weeks and 38 weeks of a high-fat diet, there was a significant increase in body weight, serum total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C) and triglycerides (TG) in mice, along with lipid accumulation in the liver, which was more severe at 38 weeks than at 16 weeks. The transcriptome data showed significant changes in the expression profile of autophagy genes in the livers of NAFLD mice following a long-term high-fat diet. Among the 31 differentially expressed autophagy-related genes, 13 were upregulated and 18 were downregulated. GO and KEGG pathway analysis revealed that these DEGs were primarily involved in autophagy, cholesterol transport, triglyceride metabolism, apoptosis, the FoxO signaling pathway, the p53 signaling pathway and the IL-17 signaling pathway. Four hub genes were identified by the PPI network analysis, of which Irs2, Pnpla2 and Plin2 were significantly downregulated, while Srebf2 was significantly upregulated by the 38-week high-fat diet. (4) The hub genes Irs2, Pnpla2, Srebf2 and Plin2 may serve as key therapeutic targets and early diagnostic markers in the progression of NAFLD. Full article

(This article belongs to the Special Issue Autophagy in Health and Diseases)

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Open AccessArticle

Autophagy Is Required to Sustain Increased Intestinal Cell Proliferation during Phenotypic Plasticity Changes in Honey Bee (Apis mellifera)

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Int. J. Mol. Sci. 2023, 24(3), 1926; https://doi.org/10.3390/ijms24031926 - 18 Jan 2023

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Abstract

Tissue phenotypic plasticity facilitates rapid adaptation of organisms to biotic and/or abiotic pressure. The reproductive capacity of honey bee workers (Apis mellifera) is plastic and responsive to pheromones produced by broods and the queen. Egg laying workers (ELWs), which could reactivate their ovaries and lay haploid eggs upon queen lost, have been commonly discussed from many aspects. However, it remains unclear whether midgut homeostasis in ELWs is affected during plastic changes. Here, we found that the expression of nutrition- and autophagy-related genes was up-regulated in the midguts of ELWs, compared with that in nurse workers (NWs) by RNA-sequencing. Furthermore, the area and number of autophagosomes were increased, along with significantly increased cell death in the midguts of ELWs. Moreover, cell cycle progression in the midguts of ELWs was increased compared with that in NWs. Consistent with the up-regulation of nutrition-related genes, the body and midgut sizes, and the number of intestinal proliferation cells of larvae reared with royal jelly (RJ) obviously increased more than those reared without RJ in vitro. Finally, cell proliferation was dramatically suppressed in the midguts of ELWs when autophagy was inhibited. Altogether, our data suggested that autophagy was induced and required to sustain cell proliferation in ELWs’ midguts, thereby revealing the critical role of autophagy played in the intestines during phenotypic plasticity changes. Full article

(This article belongs to the Special Issue Autophagy in Health and Diseases)

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Review

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Open AccessReview

Autophagy and SARS-CoV-2-Old Players in New Games

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Int. J. Mol. Sci. 2023, 24(9), 7734; https://doi.org/10.3390/ijms24097734 - 23 Apr 2023

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Abstract

At present it is well-defined that autophagy is a fundamental process essential for cell life but its pro-viral and anti-viral role has been stated out with the COVID pandemic. However, viruses in turn have evolved diverse adaptive strategies to cope with autophagy driven host defense, either by blocking or hijacking the autophagy machinery for their own benefit. The mechanisms underlying autophagy modulation are presented in the current review which summarizes the accumulated knowledge on the crosstalk between autophagy and viral infections, with a particular emphasizes on SARS-CoV-2. The different types of autophagy related to infections and their molecular mechanisms are focused in the context of inflammation. In particular, SARS-CoV-2 entry, replication and disease pathogenesis are discussed. Models to study autophagy and to formulate novel treatment approaches and pharmacological modulation to fight COVID-19 are debated. The SARS-CoV-2—autophagy interplay is presented, revealing the complex dynamics and the molecular machinery of autophagy. The new molecular targets and strategies to treat COVID-19 effectively are envisaged. In conclusion, our finding underline the importance of development new treatment strategies and pharmacological modulation of autophagy to fight COVID-19. Full article

(This article belongs to the Special Issue Autophagy in Health and Diseases)

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