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Cardiomyocyte‐generated Monocyte Chemoattractant Protein 1 Contributes to Cardiac Inflammation During Adverse Remodeling in Pressure Overload

Attempts to normalize cardiac function in response to stress often lead to cardiovascular diseases associated with adverse remodeling. Cardiac inflammation is a hallmark feature of adverse remodeling. Although it is established that ischemic injury induces cardiac inflammation through release of substances from dying cells, mechanisms for inflammation in the context of nonischemic injury have been elusive. Our lab has previously shown that the cardiomyocyte is the initial site of transcription of pro‐inflammatory cytokines and chemokines such as MCP‐1, IL‐6, Il‐1β and Il‐18, in response to pressure overload and that this occurs in the absence of cell death. In addition, the NLRP3 inflammasome is activated in cardiomyocytes resulting in activation of caspase‐1 and generation of active forms of Il‐1β and IL‐18. Pharmacological blockade of NFκ‐β, MCP‐1 signaling, or NLRP3 inflammasome activation resulted in decreases in cardiac macrophage accumulation, fibrosis, and dysfunction. These results suggest that cardiomyocyte‐generated inflammatory mediators play a key role in adverse cardiac remodeling in response to pressure overload. However, the extent to which cardiomyocytes contribute to immune cell recruitment and remodeling through MCP‐1 and inflammasome generated Il‐1β and IL‐18 remains elusive.