Preparation of controlled degradation of insulin-like growth factor 1/spider silk protein nanofibrous membrane and its effect on endothelial progenitor cell viability-Reference-Cited by-同舟云学术

Preparation of controlled degradation of insulin-like growth factor 1/spider silk protein nanofibrous membrane and its effect on endothelial progenitor cell viability

Published:2021-01-01 Issue:1 Volume:12 Page:8031-8042
ISSN:2165-5979
Container-title:Bioengineered
language:en
Short-container-title:Bioengineered

Author:

Chen Lifang¹,Huang Yulang¹,Yang Rongfeng²,Xiao Jian¹,Gao Jiajia²,Zhang Debao¹,Cao Duanwen³,Ke Xiao²⁴

Affiliation:

1. Department of Cardiology, Shenzhen Nanshan District Shekou People’ S Hospital, Shenzhen, China

2. Department of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, China

3. Clinical Trials Research Centre, The First Affiliated Hospital of Nanchang University, Nanchang China

4. Key Laboratory of Biomaterials of Guangdong Higher Education Institutes, Department of Biomedical Engineering, Jinan University, Guangzhou, China

Funder

China Postdoctoral Science Foundation

Publisher

Informa UK Limited

Subject

Applied Microbiology and Biotechnology,General Medicine,Bioengineering,Biotechnology

Link

https://www.tandfonline.com/doi/pdf/10.1080/21655979.2021.1982270

Reference46 articles.

1. Endothelial progenitor cells in ischemic stroke: an exploration from hypothesis to therapy

2. Long non-coding RNA LOC285194 regulates vascular smooth muscle cell apoptosis in atherosclerosis

3. A combination of experimental and numerical methods to investigate the role of strain rate on the mechanical properties and collagen fiber orientations of the healthy and atherosclerotic human coronary arteries

4. MicroRNA-488 serves as a diagnostic marker for atherosclerosis and regulates the biological behavior of vascular smooth muscle cells

5. PTB domain and leucine zipper motif 1 (APPL1) inhibits myocardial ischemia/hypoxia-reperfusion injury via inactivation of apoptotic protease activating factor-1 (APAF-1)/Caspase9 signaling pathway

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