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HGPS patients age and die prematurely, predominantly from cardiovascular complications. Progerin-induced cardiac repolarization defects have been described previously, although the underlying mechanisms are unknown.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>We conducted studies in heart tissue from progerin-expressing LmnaG609G\/G609G (G609G) mice, including microscopy, intracellular calcium dynamics, patch-clamping, in vivo magnetic resonance imaging, and electrocardiography.\u00a0G609G mouse cardiomyocytes showed tubulin-cytoskeleton disorganization, t-tubular system disruption, sarcomere shortening, altered excitation\u2013contraction coupling, and reductions in ventricular thickening and cardiac index. G609G mice exhibited severe bradycardia, and significant alterations of atrio-ventricular conduction and repolarization. Most importantly, 50% of G609G mice had altered heart rate variability, and sinoatrial block, both significant signs of premature cardiac aging. G609G cardiomyocytes had electrophysiological alterations, which resulted in an elevated action potential plateau and early afterdepolarization bursting, reflecting slower sodium current inactivation and long Ca+2 transient duration, which may also help explain the mild QT prolongation in some HGPS patients. Chronic treatment with low-dose paclitaxel ameliorated structural and functional alterations in G609G hearts.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our results demonstrate that tubulin-cytoskeleton disorganization in progerin-expressing cardiomyocytes causes structural, cardiac conduction, and excitation\u2013contraction coupling defects, all of which can be partially corrected by chronic treatment with low dose paclitaxel.<\/jats:p><\/jats:sec>","DOI":"10.1093\/cvr\/cvab055","type":"journal-article","created":{"date-parts":[[2021,2,19]],"date-time":"2021-02-19T13:27:57Z","timestamp":1613741277000},"page":"503-516","source":"Crossref","is-referenced-by-count":23,"title":["Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson\u2013Gilford progeria 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