Accumulation of reactive oxygen species (ROS) promotes vascular disease in obesity, but the underlying molecular mechanisms remain poorly understood. The adaptor p66Shc is emerging as a key molecule responsible for ROS generation and vascular damage. This study investigates whether epigenetic regulation of p66Shc contributes to obesity-related vascular disease.
Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity / Costantino, Sarah; Paneni, Francesco; Virdis, Agostino; Hussain, Shafaat; Mohammed, Shafeeq Ahmed; Capretti, Giuliana; Akhmedov, Alexander; Dalgaard, Kevin; Chiandotto, Sergio; Pospisilik, J Andrew; Jenuwein, Thomas; Giorgio, Marco; Volpe, Massimo; Taddei, Stefano; Lüscher, Thomas F; Cosentino, Francesco. - In: EUROPEAN HEART JOURNAL. - ISSN 1522-9645. - STAMPA. - 40:4(2017), pp. 383-391. [10.1093/eurheartj/ehx615]
Interplay among H3K9-editing enzymes SUV39H1, JMJD2C and SRC-1 drives p66Shc transcription and vascular oxidative stress in obesity
Paneni, Francesco;Capretti, Giuliana;Chiandotto, Sergio;Volpe, Massimo;Cosentino, Francesco
2017
Abstract
Accumulation of reactive oxygen species (ROS) promotes vascular disease in obesity, but the underlying molecular mechanisms remain poorly understood. The adaptor p66Shc is emerging as a key molecule responsible for ROS generation and vascular damage. This study investigates whether epigenetic regulation of p66Shc contributes to obesity-related vascular disease.| File | Dimensione | Formato | |
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