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, S., Paneni, F., Virdis, A., Hussain, S., Mohammed, S.A., Capretti, G., Akhmedov, A., Dalgaard, K., Chiandotto, S., Pospisilik, J.A., Jenuwein, T., Giorgio, M., Volpe, M., Taddei, S., Lüscher, T.F., Cosentino, F.. - 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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