Fig. 5: Summary of findings and hypothesis. | Nature Communications

Fig. 5: Summary of findings and hypothesis.

From: Testosterone exacerbates neutrophilia and cardiac injury in myocardial infarction via actions in bone marrow

Fig. 5: Summary of findings and hypothesis.

In acute MI, the surge in blood neutrophils is a result of neutrophil release from the BM, triggered by various factors, including G-CSF, which suppress the production of neutrophil retention factors, most importantly CXCL12, in the BM. Testosterone (in green) acts via the AR to reduce the production of CXCL12 from BM stromal cells. Homeostatic lower levels of CXCL12 make the BM more prone to release neutrophils in response to egress triggers. The relatively higher blood neutrophils in the presence of male levels of testosterone aggravate myocardial injury in acute MI. Actions of testosterone in men translate into sex differences in neutrophilia and protection by tocilizumab in acute MI-reperfusion. Created in BioRender. Tivesten, Å. (2024) https://BioRender.com/b63s329. G-CSF granulocyte colony-stimulating factor, IL-6 interleukin-6, AR androgen receptor, BM bone marrow.

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