Ca²⁺ dysregulation in cardiac stromal cells sustains fibro-adipose remodeling in Arrhythmogenic Cardiomyopathy and can be modulated by flecainide.

ABSTRACT:

Background

Cardiac mesenchymal stromal cells (C-MSC) were recently shown to differentiate into adipocytes and myofibroblasts to promote the aberrant remodeling of cardiac tissue that characterizes arrhythmogenic cardiomyopathy (ACM). A calcium (Ca²⁺) signaling dysfunction, mainly demonstrated in mouse models, is recognized as a mechanism impacting arrhythmic risk in ACM cardiomyocytes. Whether similar mechanisms influence ACM C-MSC fate is still unknown. Thus, we aim to ascertain whether intracellular Ca²⁺ oscillations and the Ca²⁺ toolkit are altered in human C-MSC obtained from ACM patients, and to assess their link with C-MSC-specific ACM phenotypes.

Methods and results

ACM C-MSC show enhanced spontaneous Ca²⁺ oscillations and c

SUBMITTER: Maione AS 

PROVIDER: S-EPMC9652790 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature