Skip to main content
. Author manuscript; available in PMC: 2014 Feb 12.
Published in final edited form as: J Am Coll Cardiol. 2012 Dec 5;61(6):599–610. doi: 10.1016/j.jacc.2012.08.1021

Figure 2. Targeting Mitochondrial ROS Production.

Figure 2

Mitochondrial ETC complexes and Nox4 enzyme generate excessive amounts of ROS in failing hearts. Moreover, mitochondria are very sensitive to oxidative stress and their function is severely impaired in HF. While non-specific antioxidants, such as vitamin E, show no benefit in HF, targeting of ROS-scavenging molecules to mitochondria is protective. Various approaches to targeting antioxidant compounds to mitochondria, including TPP conjugation (MitoQ), Szeto-Sciller peptides, and synthesis of novel MnSOD/Catalase mimetics, should be explored in the development of HF treatments.