ArticleMolecular medicine reports2020
High expression levels and localization of Sox5 in dilated cardiomyopathy.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Discovery ofDiagnostics (Basel, Switzerland) · 2025Article
- METTL3 mediates SOX5 m6A methylation in bronchial epithelial cells to attenuate Th2 cell differentiation in T2 asthma.Heliyon · 2024Article
- Calsyntenin-1 Promotes Doxorubicin-induced Dilated Cardiomyopathy in Rats.Cardiovascular drugs and therapy · 2024Article
- Effect of miR-499-5p/SOX6 axis on atrial fibrosis in rats with atrial fibrillation.Open medicine (Warsaw, Poland) · 2023Article
- I-κB kinase-ε deficiency improves doxorubicin-induced dilated cardiomyopathy by inhibiting the NF-κB pathway.Frontiers in physiology · 2022Article
- Regulation of Transplanted Cell Homing by FGF1 and PDGFB after Doxorubicin Myocardial Injury.Cells · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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