Key result
Intermittent hypoxia induces endothelial apoptosis via ER stress but taurodeoxycholic acid attenuates this effect.
Why the study?
Does intermittent or persistent hypoxia induce endothelial apoptosis through endoplasmic reticular stress, and can it be attenuated by taurodeoxycholic acid?
Population
24 8-week-old male Sprague Dawley rats and human umbilical vein endothelial cells of the line ECV304
Comparison
Intermittent hypoxia and persistent hypoxia… vs Normoxia (NC) group
Design
Preclinical
Follow-up
4 to 12 hours (in vitro)
Authors
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No immediate clinical implications; extends preclinical ER stress data but leaves open human translation.
Does intermittent or persistent hypoxia induce endothelial apoptosis through endoplasmic reticular stress, and can it be attenuated by taurodeoxycholic acid?
Hypoxia induces endothelial cell apoptosis via the endoplasmic reticulum stress pathway, which can be mitigated by taurodeoxycholic acid.
Yang et al. (2013) studied Endothelial apoptosis (n=24). Intermittent and persistent hypoxia vs. Normoxia was evaluated on Endothelium apoptosis and expressions of GRP78, CHOP and caspase12. Hypoxia, especially intermittent hypoxia, induced endothelial cell apoptosis via the endoplasmic reticulum stress pathway, which was attenuated by taurodeoxycholic acid.
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