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Recognition of self-DNA drives cardiac inflammation: why broken hearts fail

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Signals that govern immune cells in the heart remain poorly defined. A new report in mice shows that pathways involved in sensing viruses orchestrate monocyte and macrophage activation through recognition of DNA derived from dying cardiomyocytes following myocardial infarction.

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Figure 1: The role of cGAS–STING signaling in cardiac inflammation following myocardial infarction.

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Authors and Affiliations

  1. the Division of Cardiology, Department of Medicine, Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri, USA

    Kory J Lavine & Douglas L Mann

  2. the Departments of Developmental Biology and of Immunology and Pathology, Washington University School of Medicine, St. Louis, Missouri, USA

    Kory J Lavine

Authors
  1. Kory J Lavine
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  2. Douglas L Mann
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Correspondence to Kory J Lavine.

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The authors declare no competing financial interests.

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Lavine, K., Mann, D. Recognition of self-DNA drives cardiac inflammation: why broken hearts fail. Nat Med 23, 1400–1401 (2017). https://doi.org/10.1038/nm.4455

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