Protein kinase G I and heart failure: Shifting focus from vascular unloading to direct myocardial antiremodeling effects.
Protein kinase G I and heart failure: Shifting focus from vascular unloading to direct myocardial antiremodeling effects.
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DOI：
10.1161/circheartfailure.113.000575
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发表时间：
2013-11
期刊：
影响因子：
--
通讯作者：
Blanton RM
中科院分区：
文献类型：
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作者：
Kong Q;Blanton RM
PKGIα和PKGIβ分别在各种心血管组织中高度表达，包括血管平滑肌细胞（VSMC）、心脏和血管成纤维细胞、内皮和CM。3，4以往对PKGI的研究主要集中在了解其诱导VSMC舒张和动脉扩张的机制。这些研究已被广泛审查。1全身PKGI敲除（KO）导致异常血管松弛。5而且，PKGIα LZ相互作用结构域的选择性突变也会导致小鼠高血压和血管功能障碍。6迄今为止，已在VSMC中鉴定出多种PKGIα和PKGIβ LZ依赖性底物，1进一步支持特定PKGIα和PKGIβ LZ结构域在调节心血管功能中的关键作用。
PKGIα and PKGIβ are each highly expressed in various cardiovascular tissues, including vascular smooth muscle cells (VSMC), cardiac and vascular fibroblasts, endothelium, and CMs. 3, 4 Many prior studies of PKGI focused on understanding its mechanism of inducing VSMC relaxation and arterial dilation. These studies have been reviewed extensively. 1 Whole-body PKGI knockout (KO) leads to abnormal vascular relaxation. 5 And, selective mutation of the PKGIα LZ interaction domain in mice also produces hypertension and vascular dysfunction. 6 To date, multiple PKGIα and PKGIβ LZ-dependent substrates have been identified in VSMC, 1 further supporting a critical role of the specific PKGIα and PKGIβ LZ domains in regulating cardiovascular function.