Key result
Cyclic mechanical stretch increases TLR4 expression ~3-fold in cardiomyocytes via p38 MAPK and NF-κB.
Population
Cultured neonatal Wistar rat cardiomyocytes (from rats aged 2-3 days old)
Comparison
Cyclic mechanical stretch for 2 to 24 hours vs Control cardiomyocytes without stretch
Design
Preclinical
Follow-up
up to 24 hours
Authors
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May link mechanical overload to cardiomyocyte inflammation; leaves open TLR4 targeting in heart failure.
Effect estimate: 3.1-fold increase
Absolute Event Rate: 3.1% vs 1%
p-value: p=<0.001
Cyclic mechanical stretch upregulates TLR4 expression in cardiomyocytes via p38 MAP kinase and NF-κB pathways, which increases monocyte adherence and may contribute to inflammation in mechanically overloaded hearts.
Shyu et al. (2010) studied Cultured neonatal Wistar rat cardiomyocytes. Cyclic mechanical stretch vs. Control cells without stretch was evaluated on TLR4 protein expression (3.1-fold increase, p=<0.001). Cyclic mechanical stretch significantly increased TLR4 protein expression by 3.1-fold in cultured rat neonatal cardiomyocytes, mediated through activation of p38 MAP kinase and NF-κB pathways.
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