In hypertension, there is an increased risk of sudden cardiac death, which is associated
with acute hemodynamic fluctuations in the presence of ventricular structural remodelling.
Increased microtubule network (MTN) density (via polymerisation) or stability (via post-translational modifications, such as detyrosination or acetylation) may enhance
mechano-transduction in this setting and increase the incidence of mechanically-triggered
arrhythmias (‘mechano-arrhythmogenicity’) mediated by TRPA1.
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