Key result
Inhibition of miR-143-3p suppressed the activation of EKR5 and NF-κB pathways and up-regulated PPARδ expression in models of myocardial hypertrophy.
Why the study?
Does inhibition of miR-143-3p attenuate myocardial hypertrophy and inflammatory response in rat models and H9c2 cells?
Population
Rat models of myocardial hypertrophy induced by transverse aortic constriction in vivo, and H9c2 cells…
Comparison
Inhibition of miR-143-3p vs Control/sham or uninhibited models
Design
Preclinical
Authors
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May identify miR-143-3p as hypertrophy target; leaves open clinical translation from animal data.
Does inhibition of miR-143-3p attenuate myocardial hypertrophy and inflammatory response in rat models and H9c2 cells?
Inhibition of miR-143-3p attenuates inflammatory responses associated with myocardial hypertrophy by modulating the ERK5/PPARδ/NF-κB axis.
Yu et al. (2018) studied Myocardial hypertrophy. Inhibition of miR-143-3p was evaluated on Inflammatory response and ERK5/PPARδ/NF-κB axis activation. Inhibition of miR-143-3p suppressed the activation of EKR5 and NF-κB pathways and up-regulated PPARδ expression in models of myocardial hypertrophy.