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Endoplasmic Reticulum Stress Inhibition Enhances Liver Tolerance to Ischemia/Reperfusion

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Abstract:

In many physiopathological conditions, the cell controls its proper dysfunction via activation of the unfolded protein response to restore efficient protein synthesis and folding in the endoplasmic reticulum. However, whether the aim of unfolded protein response is to promote the cell survival, it can also lead to induction of cell death and then affect the cell fate. Recently, endoplasmic reticulum stress appeared to be critical for acute as well as chronic diseases including neurodegeneration, cardiac disease, cancer, obesity, type 2 diabetes, and ischemia/reperfusion injury. Therefore, inhibition of the endoplasmic reticulum stress could constitute a promising therapeutic strategy to limit cellular damage in pathologies such as hepatic ischemia/reperfusion.





Keywords: Cell death; cardiac disease; chemotherapy; endoplasmic reticulum; mitochondrion; neurodegeneration; physiopathological dysfunction; unfolded protein response

Document Type: Research Article

DOI: http://dx.doi.org/10.2174/092986711795590039

Publication date: May 1, 2011

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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