Sestrin2 suppression aggravates oxidative stress and apoptosis in endothelial cells subjected to pharmacologically induced endoplasmic reticulum stress

<p dir="ltr">Endoplasmic reticulum (ER) stress is an inflammatory response that contributes to endothelial cell dysfunction, a hallmark of cardiovascular diseases, in close interplay with oxidative stress. Recently, Sestrin2 (SESN2) emerged as a novel stress-inducible protein protect...

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Bibliographic Details
Main Author:	Munazza T. Fatima (17280679) (author)
Other Authors:	Maram Hasan (6672440) (author), Shahenda S. Abdelsalam (17280682) (author), Siveen K. Sivaraman (17280685) (author), Heba El-Gamal (17280688) (author), Muhammad A. Zahid (17280691) (author), Mohamed A. Elrayess (7956179) (author), Hesham M. Korashy (1474849) (author), Asad Zeidan (8879705) (author), Aijaz S. Parray (15010161) (author), Abdelali Agouni (181926) (author)
Published:	2021
Subjects:	Biological sciences Biochemistry and cell biology Biomedical and clinical sciences Cardiovascular medicine and haematology Pharmacology and pharmaceutical sciences Cardiovascular disease Endothelial dysfunction Sestrin2 Endoplasmic reticulum (ER) stress Oxidative stress Cell survival
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Sestrin2 suppression aggravates oxidative stress and apoptosis in endothelial cells subjected to pharmacologically induced endoplasmic reticulum stress

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