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.

Ca2+ dysregulation in cardiac stromal cells sustains fibro-adipose remodeling in Arrhythmogenic Cardiomyopathy and can be modulated by flecainide / A.S. Maione, P. Faris, L. Iengo, V. Catto, L. Bisonni, F. Lodola, S. Negri, M. Casella, A. Guarino, G. Polvani, M. Cerrone, C. Tondo, G. Pompilio, E. Sommariva, F. Moccia. - In: JOURNAL OF TRANSLATIONAL MEDICINE. - ISSN 1479-5876. - 20:1(2022 Nov 12), pp. 522.1-522.20. [10.1186/s12967-022-03742-8]

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

G. Polvani;C. Tondo;G. Pompilio;
2022

Abstract

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.
Arrhythmogenic cardiomyopathy; CaMKII; Calcium signalling; Cardiac mesenchymal stromal cells; Flecainide; Store-operated Ca2+ entry; Mice; Animals; Humans; Flecainide; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Myocytes, Cardiac; Calcium; Mesenchymal Stem Cells; Cardiomyopathies
Settore BIO/13 - Biologia Applicata
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/946370
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