دورية أكاديمية
Insulin-like growth factor binding protein-1 regulates HIF-1α degradation to inhibit apoptosis in hypoxic cardiomyocytes
العنوان: | Insulin-like growth factor binding protein-1 regulates HIF-1α degradation to inhibit apoptosis in hypoxic cardiomyocytes |
---|---|
المؤلفون: | Xiaoyan Tang, Huilin Jiang, Peiyi Lin, Zhenhui Zhang, Meiting Chen, Yi Zhang, Junrong Mo, Yongcheng Zhu, Ningning Liu, Xiaohui Chen |
المصدر: | Cell Death Discovery, Vol 7, Iss 1, Pp 1-12 (2021) |
بيانات النشر: | Nature Publishing Group, 2021. |
سنة النشر: | 2021 |
المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens LCC:Cytology |
مصطلحات موضوعية: | Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671 |
الوصف: | Abstract Hypoxia is important in ischemic heart disease. Excessive Insulin-like growth factor binding protein-1 (IGFBP-1) amounts are considered to harm cardiomyocytes in acute myocardial infarction. However, the mechanisms by which IGFBP-1 affects cardiomyocytes remain undefined. The present study demonstrated that hypoxia up-regulates IGFBP-1 and HIF-1α protein expression in cardiomyocytes. Subsequent assays showed that IGFBP-1 suppression decreased HIF-1α expression and inhibited hypoxia-induced apoptosis in cardiomyocytes, which was reversed by HIF-1α overexpression, indicating that HIF-1α is essential to IGFBP-1 function in cellular apoptosis. In addition, we showed that IGFBP-1 regulated HIF-1α stabilization through interacting with VHL. The present findings suggest that IGFBP-1–HIF-1α could be targeted for treating ischemic heart disease. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 2058-7716 |
Relation: | https://doaj.org/toc/2058-7716 |
DOI: | 10.1038/s41420-021-00629-3 |
URL الوصول: | https://doaj.org/article/38ce5540a2e940c4aa06efbbb60f63ef |
رقم الأكسشن: | edsdoj.38ce5540a2e940c4aa06efbbb60f63ef |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 20587716 |
---|---|
DOI: | 10.1038/s41420-021-00629-3 |