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Tillie RJHA, De Bruijn J, Perales-Patón J, et al. Partial Inhibition of the 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase-3 (PFKFB3) Enzyme in Myeloid Cells Does Not Affect Atherosclerosis. Front Cell Dev Biol. 2021;9:695684doi: 10.3389/fcell.2021.695684.
Tillie, R. J. H. A., De Bruijn, J., Perales-Patón, J., Temmerman, L., Ghosheh, Y., Van Kuijk, K., Gijbels, M. J., Carmeliet, P., Ley, K., Saez-Rodriguez, J., & Sluimer, J. C. (2021). Partial Inhibition of the 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase-3 (PFKFB3) Enzyme in Myeloid Cells Does Not Affect Atherosclerosis. Frontiers in cell and developmental biology, 9695684. https://doi.org/10.3389/fcell.2021.695684
Tillie, Renée J H A, et al. "Partial Inhibition of the 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase-3 (PFKFB3) Enzyme in Myeloid Cells Does Not Affect Atherosclerosis." Frontiers in cell and developmental biology vol. 9 (2021): 695684. doi: https://doi.org/10.3389/fcell.2021.695684
Tillie RJHA, De Bruijn J, Perales-Patón J, Temmerman L, Ghosheh Y, Van Kuijk K, Gijbels MJ, Carmeliet P, Ley K, Saez-Rodriguez J, Sluimer JC. Partial Inhibition of the 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase-3 (PFKFB3) Enzyme in Myeloid Cells Does Not Affect Atherosclerosis. Front Cell Dev Biol. 2021 Aug 12;9:695684. doi: 10.3389/fcell.2021.695684. eCollection 2021. PMID: 34458258; PMCID: PMC8387953.
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Front Cell Dev Biol. 2021 Aug 12;9:695684. doi: 10.3389/fcell.2021.695684. eCollection 2021.

Partial Inhibition of the 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase-3 (PFKFB3) Enzyme in Myeloid Cells Does Not Affect Atherosclerosis.

Frontiers in cell and developmental biology

Renée J H A Tillie, Jenny De Bruijn, Javier Perales-Patón, Lieve Temmerman, Yanal Ghosheh, Kim Van Kuijk, Marion J Gijbels, Peter Carmeliet, Klaus Ley, Julio Saez-Rodriguez, Judith C Sluimer

Affiliations

  1. Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center, Maastricht, Netherlands.
  2. Faculty of Medicine, Institute for Computational Biomedicine, Heidelberg University Hospital, Heidelberg University, Heidelberg, Germany.
  3. Institute of Experimental Medicine and Systems Biology, Rheinisch-Westfälische Technische Hochschule (RWTH) Aachen University, Aachen, Germany.
  4. La Jolla Institute for Immunology, San Diego, CA, United States.
  5. Department of Pathology, GROW-School for Oncology and Developmental Biology, Maastricht University Medical Center, Maastricht, Netherlands.
  6. Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands.
  7. Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), Leuven Cancer Institute, KU Leuven, Leuven, Belgium.
  8. State Key Laboratory of Ophthalmology, Zhongshan Opthalmic Center, Sun Yat-sen University, Guangzhou, China.
  9. Department of Biomedicine, Aarhus University, Aarhus, Denmark.
  10. Department of Bioengineering, University of California, San Diego, San Diego, CA, United States.
  11. British Heart Foundation (BHF) Centre for Cardiovascular Sciences (CVS), University of Edinburgh, Edinburgh, United Kingdom.

PMID: 34458258 PMCID: PMC8387953 DOI: 10.3389/fcell.2021.695684

Abstract

BACKGROUND: The protein 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) is a key stimulator of glycolytic flux. Systemic, partial PFKFB3 inhibition previously decreased total plaque burden and increased plaque stability. However, it is unclear which cell type conferred these positive effects. Myeloid cells play an important role in atherogenesis, and mainly rely on glycolysis for energy supply. Thus, we studied whether myeloid inhibition of PFKFB3-mediated glycolysis in

METHODS AND RESULTS: Analysis of atherosclerotic human and murine single-cell populations confirmed

CONCLUSION: Partial myeloid knockdown of PFKFB3 did not affect atherosclerosis development in advanced or early lesions. Previously reported positive effects of systemic, partial PFKFB3 inhibition on lesion stabilization, do not seem conferred by monocytes, macrophages or neutrophils. Instead, other

Copyright © 2021 Tillie, De Bruijn, Perales-Patón, Temmerman, Ghosheh, Van Kuijk, Gijbels, Carmeliet, Ley, Saez-Rodriguez and Sluimer.

Keywords: PFKFB3; atherosclerosis; dendritic cell; glycolysis; glycolysis inhibition; macrophage; myeloid cells; neutrophil

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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