Is it possible to fully recover from a severe heart attack? A recent study by scientists at UT Southwestern Medical Center in Texas, published in Science, suggests that with the help of gene editing, this may soon become reality.
A heart attack happens when blood vessels are blocked and the heart is deprived of oxygen. An estimated 1.9 crore people die because of cardiovascular problems every year.
Recently, the scientific world discovered that much of the damage caused by a heart attack is triggered by the over-activation of a gene named CaMKIIδ (calcium calmodulin-dependent protein kinase IIδ). This gene is a central mediator of several physiological processes in the heart; it has a crucial role in heart cell signalling and function. A part of CaMKIIδ protein is made up of two methionine amino acids. When these two are oxidised―because the heart is stressed―CaMKIIδ gets over-activated.
The USTW team hypothesised that if the methionines could be edited and turned into another amino acid, the oxidation process will not happen, which, in turn, would stop the over-activation of CaMKIIδ. To test this theory, the team edited CaMKIIδ in human heart cells growing in a petri dish using a CRISPR-Cas9 gene-editing system. They then placed both edited and unedited cells in a low-oxygen chamber. As expected, the unedited cells got damaged and died. The edited cells survived.
The researchers then replicated the test in live mice. They induced heart attacks in mice by restricting blood flow to their heart for 45 minutes. They then introduced edited CaMKIIδ components into the heart of a section of the mice. They observed that both gene-edited mice and some from the other batch continued to be alive after 24 hours. However, the condition of the unedited mice worsened over time. Meanwhile, the edited ones steadily improved over the next few weeks. Over time, their cardiac function became nearly the same as before the heart attack.
The CRISPR-Cas9 gene-editing system was discovered a decade ago. But until now, it has been used by scientists to correct genetic mutations responsible for the disease. The USTW researchers proved that it can be employed in a new way―by modifying a normal gene, rather than targeting a genetic mutation, to avoid a fatal situation.
The study published by the USTW researchers says that their findings could lead to a new strategy for protecting patients with heart issues. If the hypothesis holds true, we might soon be able to edit out our heart troubles.