Autophagy in Cell Survival and Growth—2nd Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 2279

Special Issue Editor


E-Mail Website
Guest Editor
Paul Albrechtsen Research Institute, CancerCare Manitoba, University of Manitoba, Winnipeg, MB, Canada
Interests: autophagy; cell death; cancer; signaling pathway; microbiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autophagy is a "self-digestion" process conserved in eukaryotic cells. During autophagy, intracellular materials (cargo), such as dysfunctional organelles, protein aggregates, lipid droplets, and microbial pathogens, are delivered to the lysosome to be degraded. Based on the transportation method, autophagy can be classified into three main types: macroautophagy, which is the most extensively studied; chaperone-mediated autophagy; and microautophagy.

Autophagy plays a critical role in cellular homeostasis and is associated with the progression of various diseases, such as cancer and neurodegenerative disorders. It primarily supports cell survival, whereby autophagic degradation generates small molecules for biosynthesis and energy production. Recent studies have shown that autophagy promotes cell growth, which refers to an increase in cell numbers, and is regulated by cell proliferation and cell survival.

This Special Issue aims to collect original research and review articles on the underlying mechanisms of the autophagy regulation of cell survival and growth in various eukaryotic cells. 

Dr. Yongqiang Chen
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • autophagy
  • cell survival
  • cell death
  • cell growth
  • proliferation

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

15 pages, 2894 KiB  
Article
Bitter Taste Receptor T2R14 and Autophagy Flux in Gingival Epithelial Cells
by Nisha Singh, Ben Ulmer, Manoj Reddy Medapati, Christine Zhang, Robert J. Schroth, Saeid Ghavami and Prashen Chelikani
Cells 2024, 13(6), 531; https://doi.org/10.3390/cells13060531 - 17 Mar 2024
Cited by 3 | Viewed by 1856
Abstract
Macroautophagy (hereafter autophagy) is a lysosomal degradation pathway that functions in nutrient recycling and as a mechanism of innate immunity. Previously, we reported a novel host–bacteria interaction between cariogenic S. mutans and bitter taste receptor (T2R14) in gingival epithelial cells (GECs), leading to [...] Read more.
Macroautophagy (hereafter autophagy) is a lysosomal degradation pathway that functions in nutrient recycling and as a mechanism of innate immunity. Previously, we reported a novel host–bacteria interaction between cariogenic S. mutans and bitter taste receptor (T2R14) in gingival epithelial cells (GECs), leading to an innate immune response. Further, S. mutans might be using the host immune system to inhibit other Gram-positive bacteria, such as S. aureus. To determine whether these bacteria exploit the autophagic machinery of GEC, it is first necessary to evaluate the role of T2R14 in modulating autophagic flux. So far, the role of T2R14 in the regulation of autophagy is not well characterized. Therefore, in this study, for the first time, we report that T2R14 downregulates autophagy flux in GECs, and T2R14 knockout increases acidic vacuoles. However, the treatments of GEC WT with a T2R14 agonist and antagonist did not lead to a significant change in acidic vacuole formation. Transmission electron microscopy morphometric results also suggested an increased number of autophagic vesicles in T2R14-knockout GEC. Further, our results suggest that S. mutans competence stimulating peptide CSP-1 showed robust intracellular calcium release and this effect is both T2R14- and autophagy protein 7-dependent. In this study, we provide the first evidence that T2R14 modulates autophagy flux in GEC. The results of the current study could help in identifying the impact of T2R in regulation of the immuno-microenvironment of GEC and subsequently oral health. Full article
(This article belongs to the Special Issue Autophagy in Cell Survival and Growth—2nd Edition)
Show Figures

Graphical abstract

Back to TopTop