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Metabolites
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Advances in Cellular Metabolism and Regulation
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Advances in Cellular Metabolism and Regulation

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 2005

Special Issue Editor

Prof. Dr. Wenjian Ma

E-Mail Website
Guest Editor
College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China
Interests: genome stability; the cellular response to drug toxicity and stresses; the implications of these processes for cancer and aging

Special Issue Information

Dear Colleagues,

Cellular metabolism is tightly regulated by various factors, such as genetic, epigenetic, environmental, and hormonal cues. Dysregulation of cellular metabolism can lead to various diseases, such as cancer, diabetes, and neurodegeneration. Therefore, understanding the mechanisms and pathways of cellular metabolism and regulation is crucial for developing novel diagnostic and therapeutic strategies. Advances in cellular metabolism and regulation is a rapidly evolving field that employs cutting-edge technologies and interdisciplinary approaches to unravel the complexity and diversity of metabolic networks and their interactions with other cellular processes. The aim of this Special Issue is to showcase the latest research findings and perspectives on cellular metabolism and regulation, covering topics such as:

  • Metabolic reprogramming and adaptation in response to stress, stimuli, or disease states;
  • Metabolic modulation by epigenetic changes, non-coding RNAs, or post-translational modifications;
  • Metabolic regulation of cell fate, differentiation, proliferation, survival, or death;
  • Metabolic crosstalk and communication between different cell types, tissues, or organs;
  • Metabolic biomarkers and targets for diagnosis, prognosis, or treatment of metabolic disorders.

Prof. Dr. Wenjian Ma
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. Metabolites 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 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

  • cellular metabolism
  • metabolic regulation
  • metabolic reprogramming
  • metabolic crosstalk
  • stress responses
  • metabolic disorders

Published Papers (2 papers)

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21 pages, 17604 KiB  
Article
Unveiling the Nexus: Cellular Metabolomics Unravels the Impact of Estrogen on Nicotinamide Metabolism in Mitigating Rheumatoid Arthritis Pathogenesis
by Swati Malik, Debolina Chakraborty, Prachi Agnihotri, Vijay Kumar and Sagarika Biswas
Metabolites 2024, 14(4), 214; https://doi.org/10.3390/metabo14040214 - 11 Apr 2024
Viewed by 422
Abstract
Rheumatoid arthritis (RA) is a metabolic joint disorder influenced by hormonal regulation, notably estrogen, which plays a cytoprotective role against inflammation. While estrogen’s impact on RA pathogenesis has been studied, the altered metabolite expression under estrogen’s influence remains unexplored. This study investigated the [...] Read more.
Rheumatoid arthritis (RA) is a metabolic joint disorder influenced by hormonal regulation, notably estrogen, which plays a cytoprotective role against inflammation. While estrogen’s impact on RA pathogenesis has been studied, the altered metabolite expression under estrogen’s influence remains unexplored. This study investigated the changes in the metabolome of synovial fibroblasts isolated from RA patients under 17β-estradiol (E2) using the liquid chromatography with tandem mass spectrometry (LC-MS/MS) approach followed by multivariate and biological pathway analysis along with in vitro validation. Results identified 3624 m/z, among which eight metabolites were significant (p < 0.05). Nicotinate and nicotinamide metabolism was found to be highly correlated with the treatment of E2, with metabolites NAD+ and 1-methynicotinamide (1-MNA) upregulated by E2 induction in RA-FLS. PharmMapper analysis identified potential gene targets of 1-MNA, which were further matched with RA gene targets, and thus, STAT1, MAPK14, MMP3, and MMP9 were concluded to be the common targets. E2 treatment affected the expression of these gene targets and ameliorated the development of oxidative stress associated with RA inflammation, which can be attributed to increased concentration of 1-MNA. Thus, an LC-MS/MS-based metabolomics study revealed the prominent role of estrogen in preventing inflammatory progression in RA by altering metabolite concentration, which can support its therapeutic capacity in remitting RA. Full article
(This article belongs to the Special Issue Advances in Cellular Metabolism and Regulation)
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16 pages, 10227 KiB  
Article
Celastrol Stabilizes Glycolipid Metabolism in Hepatic Steatosis by Binding and Regulating the Peroxisome Proliferator-Activated Receptor γ Signaling Pathway
by Mingzhu Luo, Yiting Wang, Yanyan Ma, Jingzhe Li, Jingyi Wang and Changzhen Liu
Metabolites 2024, 14(1), 64; https://doi.org/10.3390/metabo14010064 - 19 Jan 2024
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Abstract
The prevalence of nonalcoholic fatty liver disease (NAFLD) has been increasing. Obesity, insulin resistance, and lipid metabolic dysfunction are always accompanied by NAFLD. Celastrol modulates the Peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα) signaling pathways, thereby promoting lipolysis in [...] Read more.
The prevalence of nonalcoholic fatty liver disease (NAFLD) has been increasing. Obesity, insulin resistance, and lipid metabolic dysfunction are always accompanied by NAFLD. Celastrol modulates the Peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα) signaling pathways, thereby promoting lipolysis in 3T3-L1 adipocytes. In the present study, oleic-acid-induced NAFLD and differentiated 3T3-L1 preadipocytes were used as models of NAFLD and obesity to investigate the protective effect of celastrol. We investigated the impact of celastrol on hepatic steatosis caused by oleic acid (OA), as well as the associated underlying molecular pathways. To address the aforementioned questions, we used a cellular approach to analyze the signaling effects of celastrol on various aspects. These factors include the improvement in fatty liver in HepG2 cells, the differentiation of 3T3-L1 preadipocytes, glucose uptake, and the modulation of key transcriptional pathways associated with PPARγ. The administration of celastrol effectively mitigated lipid accumulation caused by OA in HepG2 cells, thereby ameliorating fatty liver conditions. Furthermore, celastrol suppressed the impacts on adipocyte differentiation in 3T3-L1 adipocytes. Additionally, celastrol exhibited the ability to bind to PPARγ and modulate its transcriptional activity. Notably, the ameliorative effects of celastrol on hepatic steatosis were reversed by rosiglitazone. According to our preliminary findings from in vitro celastrol signaling studies, PPARγ is likely to be the direct target of celastrol in regulating hepatic steatosis in HepG2 cells and adipocyte differentiation in 3T3-L1 cells. Full article
(This article belongs to the Special Issue Advances in Cellular Metabolism and Regulation)
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