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Biomedicines
Special Issues
Autophagy and Cellular Quality Control
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Autophagy and Cellular Quality Control

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 3497

Special Issue Editor

Dr. Rukmini Mukherjee

E-Mail Website
Guest Editor
Frankfurter Fachbereich Medizin, Frankfurt am Main, Germany
Interests: ubiquitin; autophagy; redox stress; mitochondrial biology; bacterial infection; innate immune signalling

Special Issue Information

Dear Colleagues,

Autophagy is important to maintain cellular homeostasis and is essential in a wide range of normal human physiological processes. It has an important role in cellular quality control of aged or damaged organelles, to remove toxic protein aggregates, to breakdown lipid droplets, and kill intracellular pathogens. These processes are collectively called selective autophagy processes since they are specific for the damaged entities which have to be removed from the cell. In such processes, selective autophagy receptors are activated on damaged organelles, marked by ubiquitin or ATG8 proteins which then activate autophagy through formation of an autophagosome which engulfs the damaged cargo and causes its lysosomal degradation. Initiation and execution of the autophagic cascade requires the stepwise recruitment of a set of at least 15 ATG proteins. It is now well established that autophagosomes can also be formed without the entire set of ATGs by non-canonical autophagy processes- LC3 associated phagocytosis (LAP), and conjugation of ATG8 to single membranes (CASM).

Selective autophagy processes also communicate with macroautophagy or bulk autophagy in the cell which is non-selective and chiefly function to maintain adequate nutrient levels in the cell. Cross-talk between autophagy and metabolism involve regulation through signalling cascades like those controlled by the kinases mTOR and AMPK. Mutations affecting genes/proteins involved in selective autophagy, upstream of the common core machinery of autophagy are involved in several neurodegenerative and autoinflammatory diseases.

We welcomed the submission of review and original research articles regarding the role of autophagy and cellular quality control in cellular homeostasis, aging, and disease.

Dr. Rukmini Mukherjee
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • selective autophagy
  • ATG proteins
  • cellular quality control
  • non-canonical autophagy
  • metabolic autophagy
  • autophagy in disease
  • autophagy receptors and adaptor proteins

Published Papers (2 papers)

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Research

23 pages, 9758 KiB  
Article
An Autophagy-Associated MITF–GAS5–miR-23 Loop Attenuates Vascular Oxidative and Inflammatory Damage in Sepsis
by Junning Cheng, Chang Ding, Huying Tang, Haonan Zhou, Mingdong Wu and Yikuan Chen
Biomedicines 2023, 11(7), 1811; https://doi.org/10.3390/biomedicines11071811 - 24 Jun 2023
Cited by 1 | Viewed by 1070
Abstract
Background: Sepsis induces GAS5 expression in the vascular endothelium, but the molecular mechanism is unclear, as is the role of GAS5 in sepsis. Methods and results: We observed that GAS5 expression in the endothelium was significantly upregulated in a sepsis mouse model. ChIP-PCR [...] Read more.
Background: Sepsis induces GAS5 expression in the vascular endothelium, but the molecular mechanism is unclear, as is the role of GAS5 in sepsis. Methods and results: We observed that GAS5 expression in the endothelium was significantly upregulated in a sepsis mouse model. ChIP-PCR and EMSA confirmed that the oxidative stress (OS)-activated MiT–TFE transcription factor (MITF, TFE3, and TFEB)-mediated GAS5 transcription. In vitro, GAS5 overexpression attenuated OS and inflammation in endothelial cells (ECs) while maintaining the structural and functional integrity of mitochondria. In vivo, GAS5 reduced tissue ROS levels, maintained vascular barrier function to reduce leakage, and ultimately attenuated sepsis-induced lung injury. Luciferase reporter assays revealed that GAS5 protected MITF from degradation by sponging miR-23, thereby forming a positive feedback loop consisting of MITF, GAS5, and miR-23. Despite the fact that the OS-activated MITF–GAS5–miR-23 loop boosted MITF-mediated p62 transcription, ECs do not need to increase mitophagy to exert mitochondrial quality control since MITF-mediated Nrf2 transcription exists. Compared to mitophagy, MITF-transcribed p62 prefers to facilitate the autophagic degradation of Keap1 through a direct interaction, thereby relieving the inhibition of Nrf2 by Keap1, indicating that MITF can upregulate Nrf2 at both the transcriptional and posttranscriptional levels. Following this, ChIP-PCR demonstrated that Nrf2 can also transcribe MITF, revealing that there is a reciprocal positive regulatory association between MITF and Nrf2. Conclusion: In sepsis, the ROS-activated MITF–GAS5–miR-23 loop integrated the antioxidant and autophagy systems through MITF-mediated transcription of Nrf2 and p62, which dynamically regulate the level and type of autophagy, as well as exert antioxidant and anti-inflammatory effects. Full article
(This article belongs to the Special Issue Autophagy and Cellular Quality Control)
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12 pages, 1542 KiB  
Communication
Total Chemical Synthesis of LC3A and LC3B Activity-Based Probes
by Yara Huppelschoten, Jens Buchardt, Thomas E. Nielsen, Aysegul Sapmaz and Gerbrand J. van der Heden van Noort
Biomedicines 2023, 11(3), 884; https://doi.org/10.3390/biomedicines11030884 - 13 Mar 2023
Cited by 1 | Viewed by 1806
Abstract
Autophagy is a conserved cellular process involved in the degradation of intercellular materials. During this process, double-membrane vesicles called autophagosomes engulf cytoplasmic components ready for degradation. A key component in the formation of autophagosomes are the autophagy-related (Atg) proteins, including microtubule-associated protein light [...] Read more.
Autophagy is a conserved cellular process involved in the degradation of intercellular materials. During this process, double-membrane vesicles called autophagosomes engulf cytoplasmic components ready for degradation. A key component in the formation of autophagosomes are the autophagy-related (Atg) proteins, including microtubule-associated protein light chain 3A (LC3A) and 3B (LC3B). After the C-terminus of LC3 is conjugated to a phospholipid, it promotes the elongation of the phagosome and provides a docking station for the delivery of proteins ready for degradation. Since dysregulation of the autophagy pathway has been associated with a variety of human diseases, components of this process have been considered as potential therapeutic targets. However, the mechanistic details of LC3-specific ligases and deconjugation enzymes are far from unraveled and chemical tools for activity profiling could aid in affording more insights into this process. Herein, we describe a native chemical ligation approach for the synthesis of two LC3 activity-based probes (ABPs). Initial studies show that the probes covalently interact with the cysteine protease ATG4B, showcasing the potential of these probes to unravel mechanistic and structural details. Full article
(This article belongs to the Special Issue Autophagy and Cellular Quality Control)
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