Shuang Zhang, Alexandre Paccalet, David Rohde, Sebastian Cremer, Maarten Hulsmans, I-Hsiu Lee, Kyle Mentkowski, Jana Grune, Maximilian J Schloss, Lisa Honold, Yoshiko Iwamoto, Yi Zheng, Miriam A Bredella, Colleen Buckless, Brian Ghoshhajra, Vikas Thondapu, Anja M van der Laan, Jan J Piek, Hans W M Niessen, Fabio Pallante, Raimondo Carnevale, Sara Perrotta, Daniela Carnevale, Oriol Iborra-Egea, Christian Muñoz-Guijosa, Carolina Galvez-Monton, Antoni Bayes-Genis, Charles Vidoudez, Sunia A Trauger, David Scadden, Filip K Swirski, Michael A Moskowitz, Kamila Naxerova, Matthias Nahrendorf
After myocardial infarction (MI), emergency hematopoiesis produces inflammatory myeloid cells that accelerate atherosclerosis and promote heart failure. Since the balance between glycolysis and mitochondrial metabolism regulates hematopoietic stem cell homeostasis, metabolic cues may influence emergency myelopoiesis. Here, we show in humans and female mice that hematopoietic progenitor cells increase fatty acid metabolism after MI. Blockade of fatty acid oxidation by deleting carnitine palmitoyltransferase ( Cpt1A ) in hematopoietic cells of Vav1 Cre/+ Cpt1A fl/fl mice limited hematopoietic progenitor proliferation and myeloid cell expansion after MI...
December 2023: Nat Cardiovasc Res