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DOI: 10.14670/HH-11-918
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Título: | Role of Ca2+ and ion channels in the regulation of apoptosis under hypoxia |
Fecha de publicación: | 2018 |
Editorial: | Universidad de Murcia. Departamento de Biología Celular e Histología |
Cita bibliográfica: | Histology and Histopathology, Vol.33, nº3, (2018) |
ISSN: | 1699-5848 0213-3911 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Hypoxia Apoptosis Ca2+ Ca2+ channels |
Resumen: | Hypoxia is a kind of common pathological condition existing in various diseases such as sleep apnea syndrome, myocardial infarction and stroke, which can precipitate the onset of diseases through inducing cell apoptosis. Ca2+ is the ubiquitous message in cell. Given the crucial role of Ca2+ in physiology, intracellular Ca2+ overload is a significant regulator of apoptosis. Numerous experiments show that hypoxia may cause changes of multiple cellular Ca2+ channels, for instance, Na+/Ca2+ Exchanger (NCX), L-type voltage dependent Ca2+ channel (L-VDCC), inositol triphosphate receptors (IP3R) and so on, which contribute to intracellular Ca2+ overload, thus eventually triggering cell apoptosis. However, the mechanisms underlying different Ca2+ channels involved in hypoxic apoptosis are complex. For example, chronic hypoxia or acute hypoxia may select different Ca2+ channels to influence cell apoptosis. In addition, intracellular Ca2+ overload may initiate different apoptotic pathways due to hypoxic duration. Furthermore, different locations in the cell of specific Ca2+ channels activated by hypoxia will determine different apoptosis signaling pathways. Moreover, activation of different Ca2+ channel isoforms will result in different outcomes of the cell under hypoxia. Hence, we aim to highlight the potential mechanisms of the main Ca2+ channels in regulation of apoptosis under hypoxic stress. |
Autor/es principal/es: | Wang, Miaohong Tan, Jin Miao, Yuyang Li, Mengmeng Zhang, Qiang |
URI: | http://hdl.handle.net/10201/118683 |
DOI: | DOI: 10.14670/HH-11-918 |
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.33, nº3 (2018) |
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Wang-33-237-246-2018.pdf | 4,51 MB | Adobe PDF | Visualizar/Abrir |
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