ArticleJournal of cellular and molecular medicine2020
The role of stretch, tachycardia and sodium-calcium exchanger in induction of early cardiac remodelling.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Physical inactivity by tail suspension alters markers of metabolism, structure, and autophagy of the mouse heart.Physiological reports · 2023Article
- β-Adrenergic Receptor Stimulation Maintains NCX-CaMKII Axis and Prevents Overactivation ofBiomedicines · 2022Article
- Loss of autophagy protein ATG5 impairs cardiac capacity in mice and humans through diminishing mitochondrial abundance and disrupting Ca2+ cycling.Cardiovascular research · 2022Article
- CaMKIIδC Drives Early Adaptive CaCirculation research · 2020Article
- The role of stretch, tachycardia and sodium-calcium exchanger in induction of early cardiac remodelling.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Stretch and tachycardia are common triggers for cardiac remodelling in various conditions, but a comparative characterization of their role in the excitation-transcription coupling (ETC) and early regulation of gene expression and structural changes is lacking. Here, we show that stretch and tachycardia directly induced hypertrophy of neonatal rat cardiac myocytes and also of non-myocytes. Both triggers induced similar patterns of hypertrophy but had largely distinct gene expression profiles. ACTA1 served as good hypertrophy marker upon stretch, while RCAN1 was found increased in response to tachycardia in a rate-dependent fashion. Mechanistically, several calcium-handling proteins, including the sodium-calcium exchanger (NCX), contributed to ETC. Phosphorylation of the calcium/calmodulin-dependent protein kinase II (CaMKII) was elevated and occurred downstream of NCX activation upon tachycardia, but not stretch. Microarray profiling revealed that stretch and tachycardia regulated around 33% and 20% genes in a NCX-dependent manner, respectively. In conclusion, our data show that hypertrophy induction by stretch and tachycardia is associated with different gene expression profiles with a significant contribution of the NCX.
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Registered trials
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