Eur Heart J：C型利钠肽在调节心脏结构和功能中起重要作用

2020-03-03 不详 MedSci原创

C型利钠肽（CNP）是一种重要的内皮源性信号物质，控制着血管内的同型酶；CNP也在心脏中表达，但该肽在心脏功能中的作用尚未明确。本研究的目的旨在利用具有CNP细胞特异性缺失的独特转基因菌株来阐明CNP在维持心脏形态和收缩性方面的中枢（病理）生理能力。本研究对野生型（WT）小鼠、心肌特异性敲除（cmCNP-/-）、内皮特异性敲除（ecCNP-/-）和成纤维特异性敲除（fbCNP-/-）CNP小鼠以及

C型利钠肽（CNP）是一种重要的内皮源性信号物质，控制着血管内的同型酶；CNP也在心脏中表达，但该肽在心脏功能中的作用尚未明确。本研究的目的旨在利用具有CNP细胞特异性缺失的独特转基因菌株来阐明CNP在维持心脏形态和收缩性方面的中枢（病理）生理能力。

本研究对野生型（WT）小鼠、心肌特异性敲除（cmCNP-/-）、内皮特异性敲除（ecCNP-/-）和成纤维特异性敲除（fbCNP-/-）CNP小鼠以及利钠肽受体敲除小鼠（NPR-B-/-和NPR-C-/-）进行了心脏结构和功能的检测。内皮特异性CNP缺失导致冠状动脉对内皮依赖性和血流介导的舒张反应受损。在体外，与WT小鼠相比，全身缺血导致cmCNP-/-和NPR-C-/-大面积梗死和功能恢复降低，但ecCNP-/-没有。在压力超负荷和交感神经过度激活诱发的心衰模型中，cmCNP-/－、fbCNP-/－、NPR-C-/－（但不是ecCNP-/－或NPR-B-/－）小鼠的心脏表型比WT小鼠更为严重，这些不良反应可以通过给WT小鼠（而不是NPR-C-/-）服用药理性CNP来补救。在分子水平上，CNP/NPR-C信号在心衰的发生中受损，但减弱了促肥大和促纤维化途径的激活。

研究结果显示，心肌细胞、内皮细胞和成纤维细胞的C型利钠肽通过激活NPR-C来协调和保护心脏结构、功能和冠状动脉反应性。

原始出处：

Amie J et al.C-type natriuretic peptide co-ordinates cardiac structure and function.Eur Heart J.2020 Mar.

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2020-03-28 jiyangfei

#重要作用#

86 0
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2020-03-05 zhaojie88

#ART#

65 0
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2020-03-05 tonychen21

#利钠肽#

121 0
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2020-03-05 slcumt

#HEART#

77 0
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2020-03-05 12498adam46暂无昵称

#心脏结构#

113 0

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