Department of Molecular Pharmacology, Shinshu University School of Medicine and Health Sciences, Matsumoto 390-8621, Japan.
Division of Cardiocirculatory Signaling, National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences, Okazaki 444-8787, Japan.
Cells. 2020 Feb 17;9(2):454. doi: 10.3390/cells9020454.
The heart flexibly changes its structure in response to changing environments and oxygen/nutrition demands of the body. Increased and decreased mechanical loading induces hypertrophy and atrophy of cardiomyocytes, respectively. In physiological conditions, these structural changes of the heart are reversible. However, chronic stresses such as hypertension or cancer cachexia cause irreversible remodeling of the heart, leading to heart failure. Accumulating evidence indicates that calcium dyshomeostasis and aberrant reactive oxygen species production cause pathological heart remodeling. Canonical transient receptor potential (TRPC) is a nonselective cation channel subfamily whose multimodal activation or modulation of channel activity play important roles in a plethora of cellular physiology. Roles of TRPC channels in cardiac physiology have been reported in pathological cardiac remodeling. In this review, we summarize recent findings regarding the importance of TRPC channels in flexible cardiac remodeling (i.e., cardiac plasticity) in response to environmental stresses and discuss questions that should be addressed in the near future.
心脏能够灵活地根据环境变化和身体对氧气/营养的需求改变其结构。机械负荷的增加和减少分别诱导心肌细胞肥大和萎缩。在生理条件下，心脏的这些结构变化是可逆的。然而，高血压或癌恶病质等慢性应激会导致心脏不可逆重塑，从而导致心力衰竭。越来越多的证据表明，钙稳态失调和异常活性氧产生导致病理性心脏重塑。经典瞬时受体电位 (TRPC) 是一种非选择性阳离子通道亚家族，其多模式激活或通道活性的调节在众多细胞生理学中发挥重要作用。TRPC 通道在病理性心脏重塑中的作用已在心脏生理学中得到报道。在这篇综述中，我们总结了最近关于 TRPC 通道在环境应激下灵活的心脏重塑（即心脏可塑性）中的重要性的发现，并讨论了在不久的将来应该解决的问题。
