Crossman David J
Department of Physiology, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland, 1142 New Zealand.
Biophys Rev. 2021 Nov 20;14(1):327-328. doi: 10.1007/s12551-021-00909-3. eCollection 2022 Feb.
Fibrosis and impaired Ca 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 Ca release that triggers contraction. T-tubule remodelling causing impaired Ca 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.
纤维化和钙信号受损是衰竭心脏的两个突出特征，通常被视为独立的实体。我们发现衰竭心脏中横管（T管）腔内的I型、III型和VI型胶原蛋白含量增加，这表明它们可能直接相关。T管是质膜内陷结构，有助于动作电位在心肌细胞深处快速传导，从而促进同步钙释放以触发收缩。射血分数降低的心力衰竭中，T管重塑导致钙释放和收缩受损，这一点已得到充分证实。然而，驱动这一机制的因素尚不清楚。在这篇评论中，我将简要概述支持过量胶原蛋白沉积驱动衰竭心脏T管重塑这一作用的证据。
