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Published on: June 14, 2016
Fibrosis and impaired Ca2+ signalling in heart failure
1Department of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland, 1142 New Zealand.
Insights
Excessive collagen in heart cells
Area of Science:
- Cardiovascular Biology
- Cardiac Physiology
- Molecular Cardiology
Background:
- Heart failure involves fibrosis and impaired calcium (Ca2+) signaling.
- Transverse (T)-tubules are crucial for cardiomyocyte excitation-contraction coupling.
- T-tubule remodeling is implicated in heart failure, but its drivers are unclear.
Purpose of the Study:
- To explore the link between collagen accumulation and T-tubule remodeling in heart failure.
- To present evidence for collagen disposition as a driver of T-tubule dysfunction.
Main Methods:
- Review of existing evidence on cardiac fibrosis and T-tubule structure.
- Analysis of collagen types (I, III, VI) localization within T-tubules.
Main Results:
- Increased collagen types I, III, and VI found within the lumen of T-tubules in failing hearts.
- This suggests a direct link between fibrosis and T-tubule abnormalities.
Conclusions:
- Excessive collagen deposition within T-tubules may drive their remodeling in heart failure.
- This mechanism offers a new perspective on the pathophysiology of cardiac dysfunction.
Abstract:
Fibrosis and impaired Ca2+ signalling are two prominent features of the failing heart that are generally considered as separate entities. Our discovery of increased amounts of collagen (types I, III, and VI) within the lumen of the transverse (T)-tubules in the failing heart suggests they may be directly linked. T-tubules are plasma membrane invaginations that facilitate a rapid transmission of the action potential deep within the myocyte where they facilitate a synchronous Ca2+ release that triggers contraction. T-tubule remodelling causing impaired Ca2+ release and contraction in heart failure with reduced ejection fraction is well established. However, what drives this mechanism is less clear. In this commentary, I will briefly outline the evidence that supports the role of excessive collagen disposition driving t-tubule remodelling in the failing heart.
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