Inflammation in non-ischemic heart disease: initiation by cardiomyocyte CaMKII and NLRP3 inflammasome signaling.

There is substantial evidence that chronic heart failure in humans and in animal models is associated with inflammation. Ischemic interventions such as myocardial infarction (MI) lead to necrotic cell death and release of damage associated molecular patterns (DAMPs), factors that signal cell damage and induce expression of pro-inflammatory chemokines and cytokines. It has recently become evident that non-ischemic interventions are also associated with increases in inflammatory genes and immune cell accumulation in the heart and that these contribute to fibrosis and ventricular dysfunction. How pro-inflammatory responses are elicited in non-ischemic heart disease which is, at least initially, not associated with cell death, is a critical unanswered question. In this review we provide evidence supporting the hypothesis that cardiomyocytes are an initiating site of inflammatory gene expression in response to non-ischemic stress. Furthermore we discuss the role of the multifunctional Ca2+/calmodulin regulated kinase, CaMKIIδ, as a transducer of stress signals to nuclear factor kappa B (NFκB) activation, expression of pro-inflammatory cytokines and chemokines, and priming and activation of the NOD-like pyrin domain-containing protein 3 (NLRP3) inflammasome in cardiomyocytes. We summarize recent evidence that subsequent macrophage recruitment, fibrosis and contractile dysfunction induced by Angiotensin II (AngII) infusion or transverse aortic constriction (TAC) are ameliorated by blockade of CaMKII, of MCP-1 / C-C chemokine receptor type 2 (CCR2) signaling, or of NLRP3 inflammasome activation.

• Publication year

  2019

• Venue

  American Journal of Physiology. Heart and Circulatory Physiology

• Publication date

  2019-11-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1152/ajpheart.00223.2019PMID 31441689PMCID PMC6879920
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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