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Título: | The regulatory role of HIF-1 in tubular epithelial cells in response to kidney injury |
Fecha de publicación: | 2020 |
Editorial: | Universidad de Murcia, Departamento de Biologia Celular e Histiologia |
Cita bibliográfica: | Histology and Histopathology Vol. 35, nº4 (2020) |
ISSN: | 0213-3911 1699-5848 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Kidney Hypoxia inducible factor-1 Tubular epithelial cell Apoptosis Autophagy Inflammation Metabolic pattern alteration Cell cycle arrest |
Resumen: | The high sensitivity to changes in oxygen tension makes kidney vulnerable to hypoxia. Both acute kidney injury and chronic kidney disease are almost always accompanied by hypoxia. Tubular epithelial cells (TECs), the dominant intrinsic cells in kidney tissue, are believed to be not only a victim in the pathological process of various kidney diseases, but also a major contributor to kidney damage. Hypoxia inducible factor- 1 (HIF-1) is the main regulator of adaptive response of cells to hypoxia. Under various clinical and experimental kidney disease conditions, HIF-1 plays a pivotal role in modulating multiple cellular processes in TECs, including apoptosis, autophagy, inflammation, metabolic pattern alteration, and cell cycle arrest. A comprehensive understanding of the mechanisms by which HIF-1 regulates these cellular processes in TECs may help identify potential therapeutic targets to improve the outcome of acute kidney injury and delay the progression of chronic kidney disease. |
Autor/es principal/es: | Qiu, Yumei Huang, Xiaowen He, Weichun |
URI: | http://hdl.handle.net/10201/125568 |
DOI: | https://doi.org/10.14670/HH-18-182 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 10 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
Aparece en las colecciones: | Vol.35, nº4 (2020) |
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Qiu-35-321-330-2020.pdf | 192,6 kB | Adobe PDF | Visualizar/Abrir |
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