Open AccessT-tubule remodelling disturbs localized β2-adrenergic signalling in rat ventricular myocytes during the progression of heart failure
Author(s) -
Sophie Schobesberger,
Peter Wright,
Sergiy Tokar,
Anamika Bhargava,
Catherine Mansfield,
Alexey V. Glukhov,
Claire Poulet,
Andrey Buzuk,
Áron Monszpart,
Markus B. Sikkel,
Siân E. Harding,
Viacheslav O. Nikolaev,
Alexander R. Lyon,
Julia Gorelik
Publication year - 2017
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvx074
Subject(s) - medicine , endocrinology , sarcolemma , myocyte , heart failure , caveolin 3 , microbiology and biotechnology , receptor , cyclic adenosine monophosphate , biology , colocalization , caveolae , signal transduction
Cardiomyocyte β2-adrenergic receptor (β2AR) cyclic adenosine monophosphate (cAMP) signalling is regulated by the receptors' subcellular location within transverse tubules (T-tubules), via interaction with structural and regulatory proteins, which form a signalosome. In chronic heart failure (HF), β2ARs redistribute from T-tubules to the cell surface, which disrupts functional signalosomes and leads to diffuse cAMP signalling. However, the functional consequences of structural changes upon β2AR-cAMP signalling during progression from hypertrophy to advanced HF are unknown.
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