J. Cesar Cardenas

Research Overview

For the past ten years, Dr. Cardenas has been studying the role of calcium release mediated by the inositol 1,4,5-trisphosphate receptor (InsP3R) in different cellular processes that include transcription, proliferation, autophagy and more recently in bioenergetics and metabolism. He has used several animal and cellular model systems and a broad number of molecular and cellular techniques that he can now pass along to the members of his laboratory to direct a large scientific project.

Dr. Cardenas's seminal work revealed that in unstimulated conditions, small InsP3R-mediated calcium release taken up by the mitochondria was essential to maintain cellular bioenergetics in all cell types. Inhibition of this signal causes an energetic stress that activates autophagy as a pro-survival mechanism. This ER-mitochondrial calcium communication has proven to be essential for the homeostasis of cancer cells, which selectively die when it is inhibited. They are further investigating the principal players involved, the signal transduction pathways underlying this communication and the effect it has on mitochondrial dynamics in several cellular models of cancer (Cardenas et al., 2016), especially in metastasis, which remains untreatable. Given the importance of mitochondria in cancer metabolism, he is interested in developing pharmacological and molecular tools to modulate mitochondrial function, which will also be applicable in other diseases with a strong mitochondrial component such as Parkinson’s, Alzheimer’s, diabetes, and obesity.