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Lipids and Lipid Metabolism in Autophagy
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Lipids and Lipid Metabolism in Autophagy

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

Deadline for manuscript submissions: closed (30 November 2019) | Viewed by 14181

Special Issue Editors

Dr. Tobias Eisenberg

E-Mail Website
Guest Editor
Institute of Molecular Biosciences, University of Graz, Humboldtstrasse 50/EG, 8010 Graz, Austria
Interests: autophagy; aging; lipid metabolism; yeast cell death
Dr. Martin Graef

E-Mail Website
Guest Editor
Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Str. 9b 50931 Cologne, Germany
Interests: autophagy; lipid metabolism; mitochondria; mitotic ageing

Special Issue Information

Dear Colleagues,

The process of autophagy emerges as a principal pathway to maintain cellular homeostasis, survival, and stress resistance during aging and age-associated disease. Allowing lysosomal degradation of proteins, protein aggregates, lipids, and (defective) organelles, autophagy serves as a mechanism of nutrient recycling and stress defense. Autophagy is under strict metabolic control and becomes activated upon nutrient starvation and other metabolic stresses. This includes the adaptation to lipid-associated stress and alterations in lipid metabolism. However, little is known about the precise role of specific lipids and lipid metabolism in the regulation of autophagy and its consequences for cellular and organismal aging. This interrelation is intricate, currently exceeds our detailed mechanistic understanding, and therefore requires suitable model systems for investigation.

The aim of this Special Issue is to collect primary research, current views, and future perspectives at the crossroads of lipids and lipid metabolism with autophagy and/or aging. We welcome research articles, reviews, and perspectives on related topics, including the role of lipids in the regulation and execution of autophagic machinery, membrane requirements for autophagy, lipophagy, the effects of dietary lipids, lipotoxic insults, and others.

We hope to give a comprehensive overview of current research activities and model systems employed in this exciting research area and also aim to provide methodological insights and current limitations through the contributions of expert laboratories.

Dr. Tobias Eisenberg
Dr. Martin Graef
Guest Editors

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
  • autophagosome
  • lipid
  • fatty acid
  • lipid metabolism
  • aging
  • lipotoxicity
  • model organism
  • dietary lipid
  • life span
  • health span

Published Papers (3 papers)

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Research

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18 pages, 4593 KiB  
Article
Autophagy Attenuation Hampers Progesterone Synthesis during the Development of Pregnant Corpus Luteum
by Zonghao Tang, Zhenghong Zhang, Hong Zhang, Yuhua Wang, Yan Zhang, Jiuhua Zhao, Hongqin Yang and Zhengchao Wang
Cells 2020, 9(1), 71; https://doi.org/10.3390/cells9010071 - 27 Dec 2019
Cited by 17 | Viewed by 3169
Abstract
The contribution of autophagy to catabolic balance has been well-established in various types of cells, whereas the involvement of autophagy in progesterone synthesis during rat pregnancy still remains unknown. Therefore, the present study was designed to evaluate the role of autophagy in progesterone [...] Read more.
The contribution of autophagy to catabolic balance has been well-established in various types of cells, whereas the involvement of autophagy in progesterone synthesis during rat pregnancy still remains unknown. Therefore, the present study was designed to evaluate the role of autophagy in progesterone production during the luteal development of pregnant rats. The results showed autophagy-related proteins was maintained at a low level on day 10 after pregnancy, significantly induced on day 16 and subsided to a relative low level on day 21, which was consistent with the changes of serum progesterone levels. The findings further indicated the contribution of autophagy to progesterone production was regulated by inactivation of Akt/mTOR signaling during the luteal development of pregnant rats in in vivo and in vitro experiments. Further investigations revealed autophagy may be involved in the surge of progesterone production in pregnant rats, as inhibition of autophagy by 3-MA compromised serum progesterone levels. Furthermore, 3-MA treatment also leveled down the number of lipid droplets in luteal cells, implying that autophagy may affect the production of progesterone by manipulating the formation of lipid droplets in luteal cells. In addition, the results suggested that mitophagy was mobilized during the primary stage of luteolysis and inhibition of autophagy promoted the increase of redundant mitochondrial and cytoplasmic cytochrome C in luteal cells of pregnant rats. Taken together, the present study indicated that autophagy-related proteins were induced by the inactivation of Akt/mTOR signaling and then contributed to the progesterone production possibly by affecting the formation of intracellular lipid droplets during the luteal development of pregnant rats. To our knowledge, this will provide a new insight into the important mechanism of autophagy regulating progesterone production in ovaries of pregnant mammals. Full article
(This article belongs to the Special Issue Lipids and Lipid Metabolism in Autophagy)
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18 pages, 2739 KiB  
Article
Transcriptional Regulation of Autophagy Genes via Stage-Specific Activation of CEBPB and PPARG during Adipogenesis: A Systematic Study Using Public Gene Expression and Transcription Factor Binding Datasets
by Mahmoud Ahmed, Trang Huyen Lai, Jin Seok Hwang, Sahib Zada, Trang Minh Pham and Deok Ryong Kim
Cells 2019, 8(11), 1321; https://doi.org/10.3390/cells8111321 - 25 Oct 2019
Cited by 16 | Viewed by 4032
Abstract
Autophagy is the cell self-eating mechanism to maintain cell homeostasis by removing damaged intracellular proteins or organelles. It has also been implicated in the development and differentiation of various cell types including the adipocyte. Several links between adipogenic transcription factors and key autophagy [...] Read more.
Autophagy is the cell self-eating mechanism to maintain cell homeostasis by removing damaged intracellular proteins or organelles. It has also been implicated in the development and differentiation of various cell types including the adipocyte. Several links between adipogenic transcription factors and key autophagy genes has been suggested. In this study, we tried to model the gene expression and their transcriptional regulation during the adipocyte differentiation using high-throughput sequencing datasets of the 3T3-L1 cell model. We applied the gene expression and co-expression analysis to all and the subset of autophagy genes to study the binding, and occupancy patterns of adipogenic factors, co-factors and histone modifications on key autophagy genes. We also analyzed the gene expression of key autophagy genes under different transcription factor knockdown adipocyte cells. We found that a significant percent of the variance in the autophagy gene expression is explained by the differentiation stage of the cell. Adipogenic master regulators, such as CEBPB and PPARG target key autophagy genes directly. In addition, the same factor may also control autophagy gene expression indirectly through autophagy transcription factors such as FOXO1, TFEB or XBP1. Finally, the binding of adipogenic factors is associated with certain patterns of co-factors binding that might modulate the functions. Some of the findings were further confirmed under the knockdown of the adipogenic factors in the differentiating adipocytes. In conclusion, autophagy genes are regulated as part of the transcriptional programs through adipogenic factors either directly or indirectly through autophagy transcription factors during adipogenesis. Full article
(This article belongs to the Special Issue Lipids and Lipid Metabolism in Autophagy)
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Review

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22 pages, 1823 KiB  
Review
Closing the Gap: Membrane Contact Sites in the Regulation of Autophagy
by Verena Kohler, Andreas Aufschnaiter and Sabrina Büttner
Cells 2020, 9(5), 1184; https://doi.org/10.3390/cells9051184 - 09 May 2020
Cited by 27 | Viewed by 6438
Abstract
In all eukaryotic cells, intracellular organization and spatial separation of incompatible biochemical processes is established by individual cellular subcompartments in form of membrane-bound organelles. Virtually all of these organelles are physically connected via membrane contact sites (MCS), allowing interorganellar communication and a functional [...] Read more.
In all eukaryotic cells, intracellular organization and spatial separation of incompatible biochemical processes is established by individual cellular subcompartments in form of membrane-bound organelles. Virtually all of these organelles are physically connected via membrane contact sites (MCS), allowing interorganellar communication and a functional integration of cellular processes. These MCS coordinate the exchange of diverse metabolites and serve as hubs for lipid synthesis and trafficking. While this of course indirectly impacts on a plethora of biological functions, including autophagy, accumulating evidence shows that MCS can also directly regulate autophagic processes. Here, we focus on the nexus between interorganellar contacts and autophagy in yeast and mammalian cells, highlighting similarities and differences. We discuss MCS connecting the ER to mitochondria or the plasma membrane, crucial for early steps of both selective and non-selective autophagy, the yeast-specific nuclear–vacuolar tethering system and its role in microautophagy, the emerging function of distinct autophagy-related proteins in organellar tethering as well as novel MCS transiently emanating from the growing phagophore and mature autophagosome. Full article
(This article belongs to the Special Issue Lipids and Lipid Metabolism in Autophagy)
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