Valentina Parra, Francisco Altamirano, Carolina P. Hernandez-Fuentes, Dan Tong, Victoriia Kyrychenko, David Rotter, Zully Pedrozo, Joseph a.. Hill, Verónica Eisner, Sergio Lavandero, Jay W. Schneider, Beverly a.. Rothermel.

Circulation Research. 2018;122: E20-e33

Imagine that you are attending a show of Trapeze at Ringside. In the middle of the show an artist falls and Ud. in less than a second to pray because the safety net is installed and running at its best capacity. Effectively, the network saves the life of the trapeze artist and now everyone can breathe easy.

A network. A network is exactly what they need from our heart cells, cardiomyocytes, to save in the event of a cardiac infarct. But not any network, This is a mesh of mitochondria. The intracellular organelle that produce energy for all vital activities of our body, It forms networks that protect cardiomyocytes die. Contrary to what we were taught in school, mitochondria have the ability to bind between if and form a network through a melting process, Optimizing the formation of ATP, molecule that serves as fuel cells. In reverse, mitochondria can divide or fisionar is and generate single mitochondria, smaller, you are not as efficient in the production of energy.

Research recently addressed by the DRA. Valentina Parra, teacher assistant of the University of Chile and contributor of the Advanced Center for chronic diseases - ACCDiS, held in conjunction with the laboratory of Dr. Rothermel in the Southwestern Medical Center of the University of Texas, He showed how the mitochondrial network is regulated by a protein known as RCAN1. This work was published in the March issue of the journal Circulation Research, one of the top 5 in the area of cardiovascular research, and that it was also an overview on the work of the Dra. Parra in his editorial. The publication has been highlighted since it explains how the absence of RCAN1 could exacerbate the effects of a myocardial infarction.

The Dra. Parra and his team used cardiomyocytes, which through molecular biology techniques do not express the protein RCAN1. The paper shows that in these cells devoid of RCAN1, the mitochondrial network is destabilized, mainly due to the activation of another protein known as DRP1 responsible for dividing the mitochondrial network. The researchers exposed cardiomyocytes ischemia/reperfusion treatment (I/R) simulated, It recreates the cardiac infarction. This procedure causes that cardiomyocytes die by metabolic disorders. When used with lower levels of RCAN1 cells, the death of cardiomyocytes subjected to I/r increased dramatically, Since mitochondrial safety net was interrupted. On the contrary, by increasing the amount of RCAN1, the mitochondrial network became more extensive and as a result the cells were more resistant to the I/r. In addition, the work of the Dra. Parra showed that cells that have destabilized mitochondrial network, due to the absence of RCAN1, a protein called calpain that help degrade structural proteins of the heart are most active. Like this, the absence of RCAN1 not only decreases the network of mitochondrial heart protection but also possibly increase its damage due to calpain after a heart attack.

The implications of the work of the Dra. Parra and his collaborators are spacious both in the field of Cardiology and in the area of neuroscience, because this mechanism is potentially the same that is activated in the brain after a stroke. At last, the Dra. Parra and his team of collaborators, also showed that stem cells from patients with Down's syndrome who have high levels of RCAN1, they have giant mitochondria with abnormally high metabolism, What could possibly explain some of the observed pathological characteristics in people who suffer from this syndrome.

Dr. Mario Bustamante
Postdoctoral ACCDIS

See interview 2018

See editorial 2018

See publication Parra