Key result
IL-1alpha stimulated human cardiac myofibroblasts to express IL-1beta, TNF-alpha, and IL-6 via specific signaling pathways, responses that were unaffected by IL-10 exposure.
Population
Human cardiac myofibroblasts (CMF) cultured from atrial biopsies from multiple patients
Comparison
Interleukin-1alpha vs Untreated cells or TNF-alpha treatment
Design
Preclinical
Follow-up
0-6 hours
Authors
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IL-1α may amplify post-MI inflammation via CMF cytokines; extends IL-10 modulation research in infarct healing.
IL-1alpha stimulates human cardiac myofibroblasts to express proinflammatory cytokines via specific signaling pathways, highlighting its potential role in acute inflammation post-myocardial infarction.
Turner et al. (2009) studied Myocardial infarction (in vitro model). Interleukin-1alpha (IL-1alpha) was evaluated on Proinflammatory cytokine (IL-1beta, TNF-alpha, IL-6) mRNA expression and secretion. IL-1alpha stimulated human cardiac myofibroblasts to express IL-1beta, TNF-alpha, and IL-6 via specific signaling pathways, responses that were unaffected by IL-10 exposure.
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