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Sox5 在扩张型心肌病中的高表达水平和定位。

High expression levels and localization of Sox5 in dilated cardiomyopathy.

机构信息

Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, P.R. China.

出版信息

Mol Med Rep. 2020 Aug;22(2):948-956. doi: 10.3892/mmr.2020.11180. Epub 2020 May 22.

DOI:10.3892/mmr.2020.11180
PMID:32468049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7339405/
Abstract

Dilated cardiomyopathy (DCM) is a disease that can lead to heart expansion and severe heart failure, but the specific pathogenesis remains unclear. Sox5 is a member of the Sox family with a key role in cardiac function. However, the role of Sox5 in DCM remains unclear. In the present study, wild‑type mice were intraperitoneally injected with doxorubicin (Dox) to induce DCM, and heart specimens from human patients with DCM were used to investigate the preliminary role of Sox5 in DCM. The present study demonstrated that, compared with control human hearts, the hearts of patients with DCM exhibited high expression levels of Sox5 and activation of the wnt/β‑catenin pathway. This result was consistent with Dox‑induced DCM in mice. Furthermore, in Dox‑treated mice, apoptosis was activated during the development of DCM. Inflammation and collagen deposition also increased in DCM mice. The results of the present study indicate that Sox5 may be associated with the development of DCM. Sox5 may be a novel potential factor that regulates DCM.

摘要

扩张型心肌病(DCM)是一种可导致心脏扩张和严重心力衰竭的疾病,但具体发病机制尚不清楚。Sox5 是 Sox 家族的成员,在心脏功能中起关键作用。然而,Sox5 在 DCM 中的作用尚不清楚。在本研究中,通过腹腔注射多柔比星(Dox)诱导野生型小鼠发生 DCM,并使用来自 DCM 患者的心脏标本来研究 Sox5 在 DCM 中的初步作用。本研究表明,与对照人心肌相比,DCM 患者的心脏 Sox5 表达水平升高,wnt/β-catenin 通路被激活。这一结果与 Dox 诱导的小鼠 DCM 一致。此外,在 Dox 处理的小鼠中,DCM 发生发展过程中激活了细胞凋亡。DCM 小鼠的炎症和胶原沉积也增加。本研究结果表明,Sox5 可能与 DCM 的发生有关。Sox5 可能是一种调节 DCM 的新型潜在因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/385402b34c85/MMR-22-02-0948-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/54e9c8e62d09/MMR-22-02-0948-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/5f4f4598f549/MMR-22-02-0948-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/cbdcca4be736/MMR-22-02-0948-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/385402b34c85/MMR-22-02-0948-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/54e9c8e62d09/MMR-22-02-0948-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/5f4f4598f549/MMR-22-02-0948-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/cbdcca4be736/MMR-22-02-0948-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f45f/7339405/385402b34c85/MMR-22-02-0948-g03.jpg

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