Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy.
Rimpy DhingraInna Rabinovich-NikitinSonny RothmanMatthew GubermanHongying GangVictoria MarguletsDavinder S JassalKeshav Narayan AlagarsamySanjiv DhingraCarla Valenzuela RipollFilio BilliaAbhinav DiwanAli JavaheriLorrie A KirshenbaumPublished in: Circulation (2022)
Our findings reveal a novel signaling axis that functionally connects the cardiotoxic effects of DOX to proteasomal degradation of TRAF2. Disruption of the critical TRAF2 survival pathway by DOX sensitizes cardiac myocytes to TNFα-mediated necrotic cell death and DOX cardiotoxicity.