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平滑肌细胞中转铁蛋白受体1缺乏可减轻高血压小鼠的血管重塑。

Transferrin receptor 1 deficiency in smooth muscle cells attenuates vascular remodeling in hypertensive mice.

作者信息

Naito Yoshiro, Sawada Hisashi, Horimatsu Tetsuo, Ohmuraya Masaki, Asakura Masanori, Ishihara Masaharu

机构信息

Department of Cardiovascular and Renal Medicine, School of Medicine, Hyogo Medical University, Nishinomiya, Japan.

Saha Cardiovascular Research Center, College of Medicine, University of Kentucky, Lexington, KY, USA.

出版信息

Hypertens Res. 2025 Aug;48(8):2263-2268. doi: 10.1038/s41440-025-02254-4. Epub 2025 Jun 9.

Abstract

Transferrin receptor 1 (TfR1), a crucial cellular iron receptor, has a variety of biological functions. We have previously reported that TfR1 abundance increases in the aortic media of hypertensive rat models. However, its role in vascular diseases remains unknown. In the present study, we generated smooth muscle cell (SMC)-specific TfR1 deficient mice and examined the impact of its deletion in mouse models of hypertension induced by angiotensin II or deoxycorticosterone acetate/salt administration. SMC-specific TfR1 deletion attenuated medial thickening and elastin fragmentation in both mouse models of hypertension. These results indicate that TfR1 in SMCs exerts a role in vascular remodeling in hypertension.

摘要

转铁蛋白受体1(TfR1)是一种关键的细胞铁受体,具有多种生物学功能。我们之前报道过,在高血压大鼠模型的主动脉中膜,TfR1的丰度会增加。然而,其在血管疾病中的作用仍不清楚。在本研究中,我们构建了平滑肌细胞(SMC)特异性TfR1缺陷小鼠,并在由血管紧张素II或醋酸脱氧皮质酮/盐给药诱导的高血压小鼠模型中,研究了TfR1缺失的影响。在这两种高血压小鼠模型中,SMC特异性TfR1缺失均减轻了中膜增厚和弹性蛋白断裂。这些结果表明,平滑肌细胞中的TfR1在高血压血管重塑中发挥作用。

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