In their study recently published inThe Journal of Physiology, Lipsettet al.(2019) attempted to explain t-tubulardefects observed in pathological cardiacremodelling during heart failure (HF) asthe result of reactivation of the fetal geneprogramme in cardiomyocytes. In fact,fetal cardiomyocytes show rudimentaryt-tubular architecture, structurally similarto t-tubules of HF cardiomyocytes. Theauthors observed that fetal t-tubules arefunctional while t-tubules of HF cardio-myocytes show defective triggering of localCa2+release. This work suggests thatreactivation of the fetal gene programmeis partly responsible for HF remodellingbut cannot completely explain t-tubulefunctional defects in HF cardiomyocytes.
Letter to the Editor / Crocini C.; Ferrantini C.; Coppini R.; Pavone F.S.; Poggesi C.; Cerbai E.; Sacconi L.. - In: THE JOURNAL OF PHYSIOLOGY. - ISSN 0022-3751. - ELETTRONICO. - 597:(2019), pp. 2965-2966. [10.1113/JP278018]
Letter to the Editor
Ferrantini C.;Coppini R.;Pavone F. S.;Poggesi C.;Cerbai E.;
2019
Abstract
In their study recently published inThe Journal of Physiology, Lipsettet al.(2019) attempted to explain t-tubulardefects observed in pathological cardiacremodelling during heart failure (HF) asthe result of reactivation of the fetal geneprogramme in cardiomyocytes. In fact,fetal cardiomyocytes show rudimentaryt-tubular architecture, structurally similarto t-tubules of HF cardiomyocytes. Theauthors observed that fetal t-tubules arefunctional while t-tubules of HF cardio-myocytes show defective triggering of localCa2+release. This work suggests thatreactivation of the fetal gene programmeis partly responsible for HF remodellingbut cannot completely explain t-tubulefunctional defects in HF cardiomyocytes.File | Dimensione | Formato | |
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