Key result
CaMKII inhibitors (AIP or KN93) suppressed cardiac fibroblast proliferation and decreased extracellular matrix secretion induced by angiotensin II or electrical field stimulation in vitro.
Population
Cultured neonatal rat cardiac fibroblasts
Design
Preclinical
Authors
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CaMKII inhibition attenuates profibrotic fibroblast responses in vitro; leaves open therapeutic translation to myocardial fibrosis.
CaMKII mediates cardiac fibroblast proliferation and extracellular matrix secretion, highlighting its potential as a therapeutic target for myocardial fibrosis.
Zhang et al. (2010) studied Myocardial fibrosis. CaMKII inhibitors (autocamtide-2-related inhibitory peptide [AIP] or KN93) was evaluated on Cardiac fibroblast proliferation and extracellular matrix (ECM) secretion. CaMKII inhibitors (AIP or KN93) suppressed cardiac fibroblast proliferation and decreased extracellular matrix secretion induced by angiotensin II or electrical field stimulation in vitro.
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