Key result
The myeloid type I interferon response to myocardial infarction begins remotely in bone marrow progenitors and is negatively regulated by Nrf2-activated steady-state cardiac macrophages.
No immediate change to post-MI care; leaves open Nrf2 modulation of myeloid IFN responses for future study.
steady-state cardiac macrophages. Our results show that IFN signaling begins in the bone marrow, implicate multiple transcriptional regulators (Tet2, Irf3, and Nrf2) in governing ISG expression, and provide a clinical biomarker (ISG score) for studying IFN signaling in patients.
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Calcagno et al. (2020) studied Myocardial infarction. Myocardial infarction vs. Steady state (pre-infarction) was evaluated on Expression of interferon-stimulated genes (ISGs) in myeloid cells. The myeloid type I interferon response to myocardial infarction begins remotely in bone marrow progenitors and is negatively regulated by Nrf2-activated steady-state cardiac macrophages.
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