Mice lacking immune cell β2-adrenergic receptors exhibited decreased proinflammatory macrophage infiltration, resulting in reduced cardiac injury, fibrosis, and hypertrophy, and improved cardiac function.
Heart failure
Deletion of immune cell β2-adrenergic receptors vs Control mice
Cardiac injury, immune cell infiltration, interstitial fibrosis, hypertrophy, and cardiac function
Immune cell β 2 -adrenergic receptors (β 2 ARs) are important for proinflammatory macrophage infiltration to the heart in a chronic isoproterenol administration model of heart failure. Mice lacking immune cell β 2 AR have decreased immune cell infiltration to their heart, primarily proinflammatory macrophage populations. This decrease culminated to decreased cardiac injury with lessened cardiomyocyte death, decreased interstitial fibrosis and hypertrophy, and improved function demonstrating that β 2 AR regulation of immune responses plays an important role in the heart’s response to persistent βAR stimulation.
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Miles A. Tanner
Missouri College
Charles A. Maitz
Missouri College
Laurel A. Grisanti
Integrative Medicine Institute
AJP Heart and Circulatory Physiology
University of Missouri
Missouri College
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Tanner et al. (Fri,) conducted a other in Heart failure. Deletion of immune cell β2-adrenergic receptors vs. Control mice was evaluated on Cardiac injury, immune cell infiltration, interstitial fibrosis, hypertrophy, and cardiac function. Mice lacking immune cell β2-adrenergic receptors exhibited decreased proinflammatory macrophage infiltration, resulting in reduced cardiac injury, fibrosis, and hypertrophy, and improved cardiac function.
synapsesocial.com/papers/6a092f034c1e2db30bd2619b — DOI: https://doi.org/10.1152/ajpheart.00243.2021