As mitochondria have an important role as ATP supplier, cellular ROS producer and apoptosis regulator, these organelles are a promising target for pharmacological intervention in the treatment and management of several diseases. Consequently, research on mitochondria-targeted drugs, which exclude other intracellular structures or extracellular processes, is becoming a hot topic. One approach to address the specific targeting is to conjugate bioactive molecules to a lipophilic cation such as the triphenylphosphonium (TPP +). In this chapter, the development of a new antioxidant based on the dietary cinnamic acid—caffeic acid—is described as well as the demonstration of its mitochondriotropic activity.
CITATION STYLE
Teixeira, J., Soares, P., Benfeito, S., Murphy, M. P., Oliveira, P. J., & Borges, F. (2015). Bridging the gap between nature and antioxidant setbacks: Delivering caffeic acid to mitochondria. Methods in Molecular Biology, 1265, 73–83. https://doi.org/10.1007/978-1-4939-2288-8_6
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