mTOR Prevents Ferroptosis in Cardiomyocytes

What differentiates ferroptosis in the heart from apoptosis and necrosis? Listen as Deputy Editor Merry Lindsey (University of Mississippi Medical Center) interviews lead author Takashi Matsui (University of Hawai'i) and content expert Lorrie Kirshenbaum (St. Boniface General Hospital Research Centre, Canada) about the exciting new study by Baba et al, one of the first to show that ferroptosis is distinct from autophagy, apoptosis and necrosis in cardiomyocytes. Ferroptosis is cell death characterized by excessive levels of iron and to iron-mediated reactive oxygen species generation. Did the authors find that glutathione peroxidase 4 (GPX4) played a role in cardiomyocyte ferroptosis? What connection did the authors find between the mTor pathway and iron-mediated cell death in cardiomyocytes? Listen, read, and view the beautiful cardiomyocyte isolation images to learn more.

 

Yuichi Baba, Jason K Higa, Briana K Shimada, Kate M. Horiuchi, Tomohiro Suhara, Motoi Kobayashi, Jonathan D. Woo, Hiroko Aoyagi, Karra S Marh, Hiroaki Kitaoka, and Takashi Matsui Protective Effects of the Mechanistic Target of Rapamycin against Excess Iron and Ferroptosis in Cardiomyocytes Am J Physiol Heart Circ Physiol, published November 10, 2017. DOI: 10.1152/ajpheart.00452.2017