Why the study?
The mechanism underlying pro-inflammatory cytokine expression in cardiac fibroblasts in response to beta-adrenergic stimulation remains to be fully elucidated.
Population
Cardiac fibroblasts isolated from adult wild-type or Arid5a knockout mice
Comparison
Beta-adrenergic stimulation vs unstimulated controls or Arid5a knockout
Design
Preclinical in vitro laboratory study
Authors
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Should not alter clinical management of cardiac inflammation; leaves open Arid5a as a β2AR-IL-6 mediator in fibroblasts.
β2-adrenergic stimulation upregulates IL-6 expression by inducing Arid5a through the cAMP/PKA/CREB pathway in adult cardiac fibroblasts, highlighting the β2AR/Arid5a/IL-6 axis as a potential target against cardiac inflammation.
Tanaka et al. (2020) studied this question.
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