Pathometabolism: Understanding Disease through Metabolism

A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Cellular Metabolism".

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Editors

Department Of Biotechnology and Biosciences, University of Milano Bicocca, 20126 Milano, Italy
Interests: cancer cell metabolism; metabolic rewiring in cancer; metabolic targeting in cancer therapy; mitochondria and cancer; PKA in cancer; hexosamine biosynthetic pathway in cancer growth and drug resistance; cancer cells computational models
Special Issues, Collections and Topics in MDPI journals
Magna Græcia University of Catanzaro
Interests: Metabolic rewiring, mitochondria, epigenetics, proteomics, Histone Non-enzymatic covalent modifications, DJ-1,
Special Issues, Collections and Topics in MDPI journals
Department of Bioinformatics and Biochemistry, BRICS, Technische Universität Braunschweig, 38106 Braunschweig, Germany
Interests: cellular metabolism; cancer metabolism; neurodegeneration; metabolomics; stable isotope assisted metabolomics; metabolic modelling

Topical Collection Information

Dear Colleagues,

This Topical Collection entitled “Pathometabolism: Understanding disease through metabolism” will collect high-quality research articles, perspectives, communications, and review articles describing metabolic alterations induced by human pathologies. We hope that your contributions will advance the field and lead to the development of new diagnostic and therapeutic regimens for human diseases. Since the Topical Collection aims to illustrate, through selected works, advancing research in cellular metabolism, we also encourage Editorial Board Members of the Cellular Metabolism Section of Cells to contribute feature papers reflecting the latest progress in their research field,  or to invite relevant experts and colleagues to submit papers.

We welcome manuscripts that emphasize phenotypic, biochemical, molecular features, and functional mechanisms through which cell or tissue metabolism influences or causes human pathologies. Relevant research topics include, but are not limited to, the following:

  • Cancer Metabolism;
  • Immunometabolism;
  • Metabolic host pathogen interaction;
  • Brain Metabolism;
  • Metabolic human disorders

Dr. Ferdinando Chiaradonna
Dr. Domenica Scumaci
Dr. Andre Wegner
Collection 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 collection 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.

Published Papers (1 paper)

2022

24 pages, 6183 KiB  
Article
Glycogen Storage Disease Phenotypes Accompanying the Perturbation of the Methionine Cycle in NDRG3-Deficient Mouse Livers
by Hyun Ahm Sohn, Dong Chul Lee, Anna Park, Minho Kang, Byoung-Ha Yoon, Chul-Ho Lee, Yong-Hoon Kim, Kyoung-Jin Oh, Cha Yeon Kim, Seong-Hwan Park, Han Koo, Hyoung-Chin Kim, Won Kee Yoon, Dae-Sik Lim, Daesoo Kim, Kyung Chan Park and Young Il Yeom
Cells 2022, 11(9), 1536; https://doi.org/10.3390/cells11091536 - 04 May 2022
Cited by 1 | Viewed by 2333
Abstract
N-Myc downstream regulated gene 3 (NDRG3) is a unique pro-tumorigenic member among NDRG family genes, mediating growth signals. Here, we investigated the pathophysiological roles of NDRG3 in relation to cell metabolism by disrupting its functions in liver. Mice with liver-specific KO of NDRG3 [...] Read more.
N-Myc downstream regulated gene 3 (NDRG3) is a unique pro-tumorigenic member among NDRG family genes, mediating growth signals. Here, we investigated the pathophysiological roles of NDRG3 in relation to cell metabolism by disrupting its functions in liver. Mice with liver-specific KO of NDRG3 (Ndrg3 LKO) exhibited glycogen storage disease (GSD) phenotypes including excessive hepatic glycogen accumulation, hypoglycemia, elevated liver triglyceride content, and several signs of liver injury. They suffered from impaired hepatic glucose homeostasis, due to the suppression of fasting-associated glycogenolysis and gluconeogenesis. Consistently, the expression of glycogen phosphorylase (PYGL) and glucose-6-phosphate transporter (G6PT) was significantly down-regulated in an Ndrg3 LKO-dependent manner. Transcriptomic and metabolomic analyses revealed that NDRG3 depletion significantly perturbed the methionine cycle, redirecting its flux towards branch pathways to upregulate several metabolites known to have hepatoprotective functions. Mechanistically, Ndrg3 LKO-dependent downregulation of glycine N-methyltransferase in the methionine cycle and the resultant elevation of the S-adenosylmethionine level appears to play a critical role in the restructuring of the methionine metabolism, eventually leading to the manifestation of GSD phenotypes in Ndrg3 LKO mice. Our results indicate that NDRG3 is required for the homeostasis of liver cell metabolism upstream of the glucose–glycogen flux and methionine cycle and suggest therapeutic values for regulating NDRG3 in disorders with malfunctions in these pathways. Full article
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