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      Metabolic-epigenetic nexus in regulation of stem cell fate

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          Abstract

          Stem cell fate determination is one of the central questions in stem cell biology, and although its regulation has been studied at genomic and proteomic levels, a variety of biological activities in cells occur at the metabolic level. Metabolomics studies have established the metabolome during stem cell differentiation and have revealed the role of metabolites in stem cell fate determination. While metabolism is considered to play a biological regulatory role as an energy source, recent studies have suggested the nexus between metabolism and epigenetics because several metabolites function as cofactors and substrates in epigenetic mechanisms, including histone modification, DNA methylation, and microRNAs. Additionally, the epigenetic modification is sensitive to the dynamic metabolites and consequently leads to changes in transcription. The nexus between metabolism and epigenetics proposes a novel stem cell-based therapeutic strategy through manipulating metabolites. In the present review, we summarize the possible nexus between metabolic and epigenetic regulation in stem cell fate determination, and discuss the potential preventive and therapeutic strategies via targeting metabolites.

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          Regulatory networks defining EMT during cancer initiation and progression.

          Bram De Craene, Geert Berx (2013)
          Epithelial to mesenchymal transition (EMT) is essential for driving plasticity during development, but is an unintentional behaviour of cells during cancer progression. The EMT-associated reprogramming of cells not only suggests that fundamental changes may occur to several regulatory networks but also that an intimate interplay exists between them. Disturbance of a controlled epithelial balance is triggered by altering several layers of regulation, including the transcriptional and translational machinery, expression of non-coding RNAs, alternative splicing and protein stability.
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            NAD+ and sirtuins in aging and disease.

            Shin-ichiro Imai, Leonard Guarente (2014)
            Nicotinamide adenine dinucleotide (NAD(+)) is a classical coenzyme mediating many redox reactions. NAD(+) also plays an important role in the regulation of NAD(+)-consuming enzymes, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38/157 ectoenzymes. NAD(+) biosynthesis, particularly mediated by nicotinamide phosphoribosyltransferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm. NAD(+) levels decline during the aging process and may be an Achilles' heel, causing defects in nuclear and mitochondrial functions and resulting in many age-associated pathologies. Restoring NAD(+) by supplementing NAD(+) intermediates can dramatically ameliorate these age-associated functional defects, counteracting many diseases of aging, including neurodegenerative diseases. Thus, the combination of sirtuin activation and NAD(+) intermediate supplementation may be an effective antiaging intervention, providing hope to aging societies worldwide. Copyright © 2014 Elsevier Ltd. All rights reserved.
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              Cardiac Energy Metabolism in Heart Failure

              Gary D. Lopaschuk, Qutuba Karwi, Rong Tian … (2021)
              Alterations in cardiac energy metabolism contribute to the severity of heart failure. However, the energy metabolic changes that occur in heart failure are complex and are dependent not only on the severity and type of heart failure present but also on the co-existence of common comorbidities such as obesity and type 2 diabetes. The failing heart faces an energy deficit, primarily because of a decrease in mitochondrial oxidative capacity. This is partly compensated for by an increase in ATP production from glycolysis. The relative contribution of the different fuels for mitochondrial ATP production also changes, including a decrease in glucose and amino acid oxidation, and an increase in ketone oxidation. The oxidation of fatty acids by the heart increases or decreases, depending on the type of heart failure. For instance, in heart failure associated with diabetes and obesity, myocardial fatty acid oxidation increases, while in heart failure associated with hypertension or ischemia, myocardial fatty acid oxidation decreases. Combined, these energy metabolic changes result in the failing heart becoming less efficient (ie, a decrease in cardiac work/O 2 consumed). The alterations in both glycolysis and mitochondrial oxidative metabolism in the failing heart are due to both transcriptional changes in key enzymes involved in these metabolic pathways, as well as alterations in NAD redox state (NAD + and nicotinamide adenine dinucleotide levels) and metabolite signaling that contribute to posttranslational epigenetic changes in the control of expression of genes encoding energy metabolic enzymes. Alterations in the fate of glucose, beyond flux through glycolysis or glucose oxidation, also contribute to the pathology of heart failure. Of importance, pharmacological targeting of the energy metabolic pathways has emerged as a novel therapeutic approach to improving cardiac efficiency, decreasing the energy deficit and improving cardiac function in the failing heart.
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                Author and article information

                Contributors
                Yi Liu
                Di-Xin Cui
                Yue Pan
                Si-Han Yu
                Li-Wei Zheng
                Mian Wan
                Journal
                Journal ID (nlm-ta): World J Stem Cells
                Journal ID (publisher-id): WJSC
                Title: World Journal of Stem Cells
                Publisher: Baishideng Publishing Group Inc
                ISSN (Electronic): 1948-0210
                Publication date (Print): 26 July 2022
                Publication date (Electronic): 26 July 2022
                Volume: 14
                Issue: 7
                Pages: 490-502
                Affiliations
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Pediatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China
                State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Cariology and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan Province, China. mianwan@ 123456scu.edu.cn
                Author notes

                Author contributions: Liu Y and Wan M conceived and designed the study; Cui DX, Pan Y and Yu SH collected materials; Liu Y wrote the paper; Zheng LW and Wan M revised the manuscript critically; all authors have read and approved the final manuscript.

                Supported by the National Natural Science Foundation of China (General Program), No. 82170921; the Sichuan Science and Technology Program, No. 2022YFS0284; and the Research and Develop Program, West China Hospital of Stomatology Sichuan University, No. LCYJ2019-24.

                Corresponding author: Mian Wan, DDS, PhD, Academic Research, Attending Doctor, Lecturer, Postdoctoral Fellow, State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Cariology and Endodontics, West China Hospital of Stomatology, Sichuan University, No. 14 People's South Road, Chengdu 610041, Sichuan Province, China. mianwan@ 123456scu.edu.cn

                Article
                Other ID: jWJSC.v14.i7.pg490
                DOI: 10.4252/wjsc.v14.i7.490
                PMC ID: 9350619
                SO-VID: 660402ad-b8a2-4bda-8022-ec2d4fdbbb2c
                Copyright © ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
                License:

                This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

                History
                Date received : 18 March 2022
                Date revision received : 31 May 2022
                Date accepted : 8 July 2022
                Categories
                Subject: Review

                Keywords: metabolism,epigenetic regulation,stem cell fate,nexus effect
                Data availability:
                Keywords: metabolism, epigenetic regulation, stem cell fate, nexus effect

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