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Journal articles on the topic 'Cell Metabolism'

To see the other types of publications on this topic, follow the link: Cell Metabolism.

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.

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2

I. Bon, Lizaveta. "The Role of Hypoxia-Induced Factor in Cell Metabolism." Journal of Obesity and Fitness Management 1, no. 1 (January 25, 2023): 01–03. http://dx.doi.org/10.58489/2836-5070/003.

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Objective. Analysis and synthesis of literature data on morphological and functional properties and the diagnostic value of induced factor hypoxia. Methods. The basis of this study was a review of literature on this topic. Results. An important role in the adaptation of the organism to hypoxia belongs to a specific regulatory protein - hypoxia-induced factor (HIF), the activity of which increases with decreasing oxygen tension in the blood. HIF is a heterodimeric protein, the beta subunit of which is constantly expressed, and the synthesis of the alpha subunit is regulated by oxygen. Conclusion. Acute oxygen deficiency is the basis of a variety of pathological processes in many diseases and environmental factors. The hypoxia-induced factor is responsible for the formation of long-term adaptation to hypoxia, and therefore is a suitable target for pharmacological effects. The search for drugs that act as inducers or inhibitors of its synthesis is an important area in experimental pharmacology, since it allows not only to regulate the processes of adaptation to hypoxia, but more effectively treat cerebrovascular, cardiovascular, oncological and other diseases in whose genesis the leading role plays oxygen deficiency.

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3

Isogai, Tadamoto, Jin Suk Park, and Gaudenz Danuser. "Cell forces meet cell metabolism." Nature Cell Biology 19, no. 6 (May 31, 2017): 591–93. http://dx.doi.org/10.1038/ncb3542.

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4

Romero-Garcia, Susana, Jose Sullivan Lopez-Gonzalez, José Luis B´ez-Viveros, Dolores Aguilar-Cazares, and Heriberto Prado-Garcia. "Tumor cell metabolism." Cancer Biology & Therapy 12, no. 11 (December 2011): 939–48. http://dx.doi.org/10.4161/cbt.12.11.18140.

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5

Cairns, R. A., I. Harris, S. McCracken, and T. W. Mak. "Cancer Cell Metabolism." Cold Spring Harbor Symposia on Quantitative Biology 76 (January 1, 2011): 299–311. http://dx.doi.org/10.1101/sqb.2011.76.012856.

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6

Teuwen, Laure-Anne, Nihed Draoui, Charlotte Dubois, and Peter Carmeliet. "Endothelial cell metabolism." Current Opinion in Hematology 24, no. 3 (May 2017): 240–47. http://dx.doi.org/10.1097/moh.0000000000000335.

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7

Pearce, Edward J., and Bart Everts. "Dendritic cell metabolism." Nature Reviews Immunology 15, no. 1 (December 23, 2014): 18–29. http://dx.doi.org/10.1038/nri3771.

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8

Eelen, Guy, Pauline de Zeeuw, Lucas Treps, Ulrike Harjes, Brian W. Wong, and Peter Carmeliet. "Endothelial Cell Metabolism." Physiological Reviews 98, no. 1 (January 1, 2018): 3–58. http://dx.doi.org/10.1152/physrev.00001.2017.

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Endothelial cells (ECs) are more than inert blood vessel lining material. Instead, they are active players in the formation of new blood vessels (angiogenesis) both in health and (life-threatening) diseases. Recently, a new concept arose by which EC metabolism drives angiogenesis in parallel to well-established angiogenic growth factors (e.g., vascular endothelial growth factor). 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3-driven glycolysis generates energy to sustain competitive behavior of the ECs at the tip of a growing vessel sprout, whereas carnitine palmitoyltransferase 1a-controlled fatty acid oxidation regulates nucleotide synthesis and proliferation of ECs in the stalk of the sprout. To maintain vascular homeostasis, ECs rely on an intricate metabolic wiring characterized by intracellular compartmentalization, use metabolites for epigenetic regulation of EC subtype differentiation, crosstalk through metabolite release with other cell types, and exhibit EC subtype-specific metabolic traits. Importantly, maladaptation of EC metabolism contributes to vascular disorders, through EC dysfunction or excess angiogenesis, and presents new opportunities for anti-angiogenic strategies. Here we provide a comprehensive overview of established as well as newly uncovered aspects of EC metabolism.

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9

Gardiner, Clair M. "NK cell metabolism." Journal of Leukocyte Biology 105, no. 6 (January 24, 2019): 1235–42. http://dx.doi.org/10.1002/jlb.mr0718-260r.

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10

Verdegem, Dries, Stijn Moens, Peter Stapor, and Peter Carmeliet. "Endothelial cell metabolism: parallels and divergences with cancer cell metabolism." Cancer & Metabolism 2, no. 1 (2014): 19. http://dx.doi.org/10.1186/2049-3002-2-19.

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11

Prokopcová, Adéla. "(Energetic metabolism of endothelial cell)." Cor et Vasa 61, no. 3 (June 21, 2019): e294-e298. http://dx.doi.org/10.33678/cor.2019.027.

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12

Haraguchi, Misako, Hiroko P. Indo, Yasumasa Iwasaki, Yoichiro Iwashita, Tomoko Fukushige, Hideyuki J. Majima, Kimiko Izumo, et al. "Snail modulates cell metabolism in MDCK cells." Biochemical and Biophysical Research Communications 432, no. 4 (March 2013): 618–25. http://dx.doi.org/10.1016/j.bbrc.2013.02.035.

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13

Plathow, C., and W. A. Weber. "Tumor Cell Metabolism Imaging." Journal of Nuclear Medicine 49, Suppl_2 (June 1, 2008): 43S—63S. http://dx.doi.org/10.2967/jnumed.107.045930.

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14

Santelia, Diana, and Tracy Lawson. "Rethinking Guard Cell Metabolism." Plant Physiology 172, no. 3 (September 8, 2016): 1371–92. http://dx.doi.org/10.1104/pp.16.00767.

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15

Kaelin, William G., and Craig B. Thompson. "Clues from cell metabolism." Nature 465, no. 7298 (June 2010): 562–64. http://dx.doi.org/10.1038/465562a.

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16

Bradley, Conor A. "FGFR1 reprogrammes cell metabolism." Nature Reviews Urology 15, no. 9 (June 26, 2018): 528. http://dx.doi.org/10.1038/s41585-018-0053-6.

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17

Thornton, S. N., P. C. Even, and G. van Dijk. "Hydration increases cell metabolism." International Journal of Obesity 33, no. 3 (January 20, 2009): 385. http://dx.doi.org/10.1038/ijo.2008.264.

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18

Kobayashi, Takumi, and Stephen R. Mattarollo. "Natural killer cell metabolism." Molecular Immunology 115 (November 2019): 3–11. http://dx.doi.org/10.1016/j.molimm.2017.11.021.

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19

B.M.W. "Fibrosis and cell metabolism." Human Pathology 18, no. 11 (November 1987): 1083–84. http://dx.doi.org/10.1016/s0046-8177(87)80372-6.

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20

Dempsey, Laurie A. "B-1a cell metabolism." Nature Immunology 19, no. 3 (February 23, 2018): 206. http://dx.doi.org/10.1038/s41590-018-0060-z.

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21

Bates, Susan E. "Reinventing Cancer Cell Metabolism." Clinical Cancer Research 18, no. 20 (October 14, 2012): 5536. http://dx.doi.org/10.1158/1078-0432.ccr-12-2884.

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22

Cain, Chris. "Targeting T cell metabolism." Science-Business eXchange 4, no. 9 (March 2011): 243. http://dx.doi.org/10.1038/scibx.2011.243.

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23

Chakradhar Challagali, Sri. "Warburg Effect and its Role in Cancer Cell Metabolism: A Comprehensive Review." International Journal of Science and Research (IJSR) 12, no. 6 (June 5, 2023): 500–504. http://dx.doi.org/10.21275/sr23602104158.

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24

Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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25

Rigaud, Vagner O. C., Robert Hoy, Sadia Mohsin, and Mohsin Khan. "Stem Cell Metabolism: Powering Cell-Based Therapeutics." Cells 9, no. 11 (November 16, 2020): 2490. http://dx.doi.org/10.3390/cells9112490.

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Cell-based therapeutics for cardiac repair have been extensively used during the last decade. Preclinical studies have demonstrated the effectiveness of adoptively transferred stem cells for enhancement of cardiac function. Nevertheless, several cell-based clinical trials have provided largely underwhelming outcomes. A major limitation is the lack of survival in the harsh cardiac milieu as only less than 1% donated cells survive. Recent efforts have focused on enhancing cell-based therapeutics and understanding the biology of stem cells and their response to environmental changes. Stem cell metabolism has recently emerged as a critical determinant of cellular processes and is uniquely adapted to support proliferation, stemness, and commitment. Metabolic signaling pathways are remarkably sensitive to different environmental signals with a profound effect on cell survival after adoptive transfer. Stem cells mainly generate energy through glycolysis while maintaining low oxidative phosphorylation (OxPhos), providing metabolites for biosynthesis of macromolecules. During commitment, there is a shift in cellular metabolism, which alters cell function. Reprogramming stem cell metabolism may represent an attractive strategy to enhance stem cell therapy for cardiac repair. This review summarizes the current literature on how metabolism drives stem cell function and how this knowledge can be applied to improve cell-based therapeutics for cardiac repair.

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26

Westerhoff, Hans V. "Cell metabolism: Organization in the cell soup." Nature 318, no. 6042 (November 1985): 106. http://dx.doi.org/10.1038/318106a0.

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27

Buchanan, M. R., M. C. Bertomeu, and E. Bastida. "Fatty acid metabolism and cell/cell interactions." Agents and Actions 29, no. 1-2 (January 1990): 16–20. http://dx.doi.org/10.1007/bf01964707.

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28

Fulda, Simone. "Alternative Cell Death Pathways and Cell Metabolism." International Journal of Cell Biology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/463637.

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While necroptosis has for long been viewed as an accidental mode of cell death triggered by physical or chemical damage, it has become clear over the last years that necroptosis can also represent a programmed form of cell death in mammalian cells. Key discoveries in the field of cell death research, including the identification of critical components of the necroptotic machinery, led to a revised concept of cell death signaling programs. Several regulatory check and balances are in place in order to ensure that necroptosis is tightly controlled according to environmental cues and cellular needs. This network of regulatory mechanisms includes metabolic pathways, especially those linked to mitochondrial signaling events. A better understanding of these signal transduction mechanisms will likely contribute to open new avenues to exploit our knowledge on the regulation of necroptosis signaling for therapeutic application in the treatment of human diseases.

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29

Leal-Esteban, Lucia C., and Lluis Fajas. "Cell cycle regulators in cancer cell metabolism." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1866, no. 5 (May 2020): 165715. http://dx.doi.org/10.1016/j.bbadis.2020.165715.

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30

Tronko, M. D., V. M. Pushkarev, E. I. Kovzun, L. K. Sokolova, and V. V. Pushkarev. "Epigenetics, cell cycle and stem cell metabolism. Formation of insulin-producing cells." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 18, no. 3 (June 20, 2022): 169–79. http://dx.doi.org/10.22141/2224-0721.18.3.2022.1165.

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Stem cell (SC) differentiation requires a series of chromatin rearrangements to establish cell identity. Posttranslational modifications of histones usually regulate the dynamics of heterochromatin. Histones are subjected to various modifications, such as acetylation, methylation, phosphorylation and ubiquinination, and thus contribute to regulation of chromatin status and transcriptional activity. The chemically stable pattern of methylated histones promotes cellular memory relative to external stimuli, maintaining transcription levels of adaptive genes even after elimination of environmental signals. Chromatin modifications play an important role in the maturation of pancreatic islet cells, the establishment of a secretion pattern that stimulates the regulation of insulin secretion. MicroRNAs, a class of endogenous small noncoding RNAs in eukaryotes, are important regulators of gene expression at the level of posttranscriptional mechanisms. MicroRNAs regulate insulin secretion, pancreatic development, and β-cell differentiation. Pluripotent SCs are characterized by a high rate of proliferation, the ability to self-repair and the potential for differentiation in different cell types. This rapid proliferation is due to a modified cell cycle that allows cells to rapidly transition from DNA synthesis to cell division by reducing the time of gap (G1 and G2) phases. The canonical WNT/β-catenin signaling pathway is characterized as a major driver of cell growth and proliferation. At G1, WNT signaling induces a transition to the S-phase. Compared to their somatic counterparts, pluripotent SCs exhibit a high rate of glycolysis similar to aerobic glycolysis in cancer cells, a phenomenon known as the Warburg effect, which is important for maintaining SC properties. In stem cells, the extracellular influx of Ca2+ into the cytoplasm is mediated mainly by depot-controlled Ca2+ channels. Extracellular calcium has been shown to promote SC proliferation and thus may be involved in transplant therapy.

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31

Chatterjee, Payal, Mukesh Yadav, Namrata Chauhan, Ying Huang, and Yun Luo. "Cancer Cell Metabolism Featuring Nrf2." Current Drug Discovery Technologies 17, no. 3 (July 15, 2020): 263–71. http://dx.doi.org/10.2174/1570163815666180911092443.

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Although the major role of Nrf2 has long been established as a transcription factor for providing cellular protection against oxidative stress, multiple pieces of research and reviews now claim exactly the opposite. The dilemma - “to activate or inhibit” the protein requires an immediate answer, which evidently links cellular metabolism to the causes and purpose of cancer. Profusely growing cancerous cells have prolific energy requirements, which can only be fulfilled by modulating cellular metabolism. This review highlights the cause and effect of Nrf2 modulation in cancer that in turn channelize cellular metabolism, thereby fulfilling the energy requirements of cancer cells. The present work also highlights the purpose of genetic mutations in Nrf2, in relation to cellular metabolism in cancer cells, thus pointing out a newer approach where parallel mutations may be the key factor to decide whether to activate or inhibit Nrf2.

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32

TAKAYAMA, Hiroshi. "Arachidonate Metabolism of Vascular Cell." Japanese Journal of Thrombosis and Hemostasis 2, no. 4 (1991): 265–73. http://dx.doi.org/10.2491/jjsth.2.265.

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33

D. Méndez, José. "Polyamine Metabolism in Sperm Cell." Diabetes & its Complications 2, no. 2 (June 30, 2018): 1–3. http://dx.doi.org/10.33425/2639-9326.1028.

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34

Buck, Michael D., David O’Sullivan, and Erika L. Pearce. "T cell metabolism drives immunity." Journal of Experimental Medicine 212, no. 9 (August 10, 2015): 1345–60. http://dx.doi.org/10.1084/jem.20151159.

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Lymphocytes must adapt to a wide array of environmental stressors as part of their normal development, during which they undergo a dramatic metabolic remodeling process. Research in this area has yielded surprising findings on the roles of diverse metabolic pathways and metabolites, which have been found to regulate lymphocyte signaling and influence differentiation, function and fate. In this review, we integrate the latest findings in the field to provide an up-to-date resource on lymphocyte metabolism.

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35

BJÖRNTORP, PER. "Fat Cell Distribution and Metabolism." Annals of the New York Academy of Sciences 499, no. 1 (December 17, 2006): 66–72. http://dx.doi.org/10.1111/j.1749-6632.1987.tb36198.x.

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36

GAO, Ping, and HaoRan WEI. "Regulation of cancer cell metabolism." SCIENTIA SINICA Vitae 47, no. 1 (January 1, 2017): 132–39. http://dx.doi.org/10.1360/n052016-00334.

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37

Käding, Nadja, Márta Szaszák, and Jan Rupp. "Imaging ofChlamydiaand host cell metabolism." Future Microbiology 9, no. 4 (April 2014): 509–21. http://dx.doi.org/10.2217/fmb.14.13.

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38

Esteban-Martínez, Lorena, Elena Sierra-Filardi, and Patricia Boya. "Mitophagy, metabolism, and cell fate." Molecular & Cellular Oncology 4, no. 5 (July 17, 2017): e1353854. http://dx.doi.org/10.1080/23723556.2017.1353854.

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39

Teng, X., W. Li, C. Cornaby, and L. Morel. "Immune cell metabolism in autoimmunity." Clinical & Experimental Immunology 197, no. 2 (March 11, 2019): 181–92. http://dx.doi.org/10.1111/cei.13277.

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40

Yoo, Hee Chan, Ya Chun Yu, Yulseung Sung, and Jung Min Han. "Glutamine reliance in cell metabolism." Experimental & Molecular Medicine 52, no. 9 (September 2020): 1496–516. http://dx.doi.org/10.1038/s12276-020-00504-8.

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Abstract As knowledge of cell metabolism has advanced, glutamine has been considered an important amino acid that supplies carbon and nitrogen to fuel biosynthesis. A recent study provided a new perspective on mitochondrial glutamine metabolism, offering mechanistic insights into metabolic adaptation during tumor hypoxia, the emergence of drug resistance, and glutaminolysis-induced metabolic reprogramming and presenting metabolic strategies to target glutamine metabolism in cancer cells. In this review, we introduce the various biosynthetic and bioenergetic roles of glutamine based on the compartmentalization of glutamine metabolism to explain why cells exhibit metabolic reliance on glutamine. Additionally, we examined whether glutamine derivatives contribute to epigenetic regulation associated with tumorigenesis. In addition, in discussing glutamine transporters, we propose a metabolic target for therapeutic intervention in cancer.

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41

Hagel-Bradway, S., and R. Dziak. "Regulation of bone cell metabolism." Journal of Oral Pathology and Medicine 18, no. 6 (July 1989): 344–51. http://dx.doi.org/10.1111/j.1600-0714.1989.tb01564.x.

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42

Huang, D., C. Li, and H. Zhang. "Hypoxia and cancer cell metabolism." Acta Biochimica et Biophysica Sinica 46, no. 3 (January 3, 2014): 214–19. http://dx.doi.org/10.1093/abbs/gmt148.

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43

Sun, Xinghui, and Mark W. Feinberg. "Regulation of Endothelial Cell Metabolism." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 1 (January 2015): 13–15. http://dx.doi.org/10.1161/atvbaha.114.304869.

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44

BERRIDGE, M. J. "Cell Signalling Through Phospholipid Metabolism." Journal of Cell Science 1986, Supplement 4 (January 1, 1986): 137–53. http://dx.doi.org/10.1242/jcs.1986.supplement_4.9.

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45

Buck, Michael D., David O'Sullivan, and Erika L. Pearce. "T cell metabolism drives immunity." Journal of Cell Biology 210, no. 4 (August 17, 2015): 2104OIA169. http://dx.doi.org/10.1083/jcb.2104oia169.

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46

Lozy, Fred, and Vassiliki Karantza. "Autophagy and cancer cell metabolism." Seminars in Cell & Developmental Biology 23, no. 4 (June 2012): 395–401. http://dx.doi.org/10.1016/j.semcdb.2012.01.005.

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47

Chang-Li, Xie, Sun Day-Ung, Song Zhau-Hua, Qu Song-Sheng, Liao Yao-Ting, and Liu Hai-Shui. "Thermochemical studies on cell metabolism." Thermochimica Acta 158, no. 1 (February 1990): 187–93. http://dx.doi.org/10.1016/0040-6031(90)80066-8.

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48

Halliwell, B. "Red cell metabolism, third edition." FEBS Letters 190, no. 1 (October 7, 1985): 173. http://dx.doi.org/10.1016/0014-5793(85)80453-1.

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49

Barford, JP, PJ Phillips, and C. Harbour. "Simulation of animal cell metabolism." Mathematics and Computers in Simulation 33, no. 5-6 (April 1992): 397–402. http://dx.doi.org/10.1016/0378-4754(92)90128-4.

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50

Barford, John P., Peter J. Phillips, and Colin Harbour. "Simulation of animal cell metabolism." Cytotechnology 10, no. 1 (1992): 63–74. http://dx.doi.org/10.1007/bf00376101.

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