Cleaning of vessels

Revolutionary development of atherosclerosis therapy

The Attending Physician Magazine

Yale University and MIT, giants of American science, are exploring new possible treatments for atherosclerosis. Their new discoveries promise a fundamentally new therapeutic approach not only to curb the progression of atherosclerosis, but also to its potential cure.

Article by Chen et al. Endothelial TGF-β signaling drives vascular inflammation and atherosclerosis is published in the journal Nature Metabolism.

Modern therapy of atherosclerotic plaques and arterial endothelial seals can only slow down the disease, but not reverse it. It is believed that the pathogenesis of atherosclerosis is primarily associated with chronic inflammation occurring in vascular tissues. One of the leading factors of this inflammation is a group of proteins called transforming growth factors beta (transforming growth factor beta, TGFß). 

Scientists examined the culture of human endothelial cells and confirmed that TGFß is indeed a trigger of inflammation in this type of cell, but it does not induce an inflammatory process in other cells, moreover, these cytokines often weaken inflammation. When the gene responsible for TGFß receptors was removed, inflammation and plaque formation in endothelial cells significantly decreased. 

In order to use this approach as a potential therapeutic one, the research team used interfering RNA (RNAi) developed at Yale University. It uses a special DNA sequence to disable the gene responsible for the TGFß receptors. To deliver this drug directly into the vascular endothelial cells of mice, they used special nanoparticles created by colleagues from MIT. This strategy proved to be as effective as gene removal in cell culture.

This discovery demonstrates the crucial role of TGFß as a factor of chronic inflammation in vascular endothelium and as an important therapeutic target in the treatment of atherosclerosis. Now scientists have launched a biotech company VasoRX to further improve the method.

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