Key result
This review summarizes changes in contraction and calcium handling during early cardiac remodeling, focusing on findings from multicellular and individual cell in vitro model systems.
This review summarizes the mechanisms of contraction and calcium handling dysregulation during early cardiac remodeling in in vitro models.
May inform preclinical targeting of early remodeling; leaves open clinical translation from in vitro models.
Cardiac remodeling, hypertrophy, and alterations in calcium signaling are changes of the heart that often lead to failure. After a hypertrophic stimulus, the heart progresses through a state ofcompensated hypertrophy which over time leads to decompensated hypertrophy or failure. It is at this point that a cardiac transplant is required for survival making early detection imperative. Current experimental systems used to study the remodeling of the heart include in vivo systems (the whole body), isolated organ and sub-organ tissue, and the individual cardiac muscle cells and organelles.. During pathological remodeling there is a derangement in the intracellular calcium handling processes. These derangements are thought to lead to a dysregulation of contractile output. Hence, understanding the mechanism between remodeling and dysregulation is of great interest in the cardiac field and will ultimately help in the development of future treatment and early detection. This review will center on changes in contraction and calcium handling in early cardiac remodeling, with a specific focus on findings in two different in vitro model systems: multicellular and individual cell preparations.
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Paul M.L. Janssen (2011) conducted a review in Cardiac remodeling and hypertrophy. In vitro model systems (multicellular and individual cell preparations) was evaluated. This review summarizes changes in contraction and calcium handling during early cardiac remodeling, focusing on findings from multicellular and individual cell in vitro model systems.
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