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Inducible Depletion of Calpain-2 Mitigates Abdominal Aortic Aneurysm in Mice
bioRxiv - Pathology Pub Date : 2020-04-15 , DOI: 10.1101/2020.04.15.043687
Latha Muniappan , Michihiro Okuyama , Aida Javidan , Devi Thiagarajan , Weihua Jiang , Jessica J. Moorleghen , Lihua Yang , Anju Balakrishnan , Deborah A. Howatt , Haruhito A. Uchida , Takaomi C. Saido , Venkateswaran Subramanian

BACKGROUND Cytoskeletal structural proteins maintain cell structural integrity by bridging extracellular matrix (ECM) with contractile filaments. During AAA development, (i) aortic medial degeneration is associated with loss of smooth muscle cell (SMC) integrity, and (ii) fibrogenic mesenchymal cells (FMSCs) mediates ECM remodeling. Calpains cleave cytoskeletal proteins that maintain cell structural integrity. Pharmacological inhibition of calpains exert beneficial effects on Angiotensin II (AngII)-induced AAAs in low density receptor deficient (LDLR-/-) mice.

中文翻译:

钙蛋白酶2的诱导耗竭减轻小鼠腹主动脉瘤。

背景技术细胞骨架结构蛋白通过用收缩性细丝桥接细胞外基质(ECM)来维持细胞结构完整性。在AAA发展过程中,(i)主动脉内侧变性与平滑肌细胞(SMC)完整性丧失有关,以及(ii)纤维化间充质细胞(FMSC)介导ECM重塑。钙蛋白酶裂解维持细胞结构完整性的细胞骨架蛋白。钙蛋白酶的药理抑制作用在低密度受体缺陷型(LDLR-/-)小鼠中对血管紧张素II(AngII)诱导的AAA产生有益作用。
更新日期:2020-04-15
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