Cardiac hypertrophy is an abnormal thickening of the heart muscle. It develops in response to constant exposure to increased stress on the heart. Cardiac hypertrophy is characterized by a thickening of the walls of the heart. The chambers of the heart become smaller, and the heart muscle loses elasticity, impairing the heart's ability to pump blood. Meanwhile, cardiac hypertrophy is also a major risk factor for cardiomyopathy, which is a serious condition that often leads to heart failure and death.
New research reveals the role a very specific protein plays in the development of cardiac hypertrophy for the first time. Specific genes are responsible for determining cell growth and differentiation during the early stages of cardiac development. Reactivation of these genes later in life can lead to an abnormal thickening of the heart muscle.
The researchers identified that a specific protein, DPF, and its splice variant, DPF3a, play a important role. Initial activation of DPF3a, which occurs as a result of phosphorylation, is achieved via the action of a special type of enzyme called a kinase. Once activated, DPF3a binds to a transcriptional repressor, a protein that inhibits the expression of different genes within the cell's DNA. Binding releases the repressor protein, thus allowing the previously blocked gene to be transcribed and translated into proteins. This action by DPF3a leads to an increase in the production of proteins that are normally associated with early cardiac development, and which are typically found in patients with cardiac hypertrophy. After analysing cardiac tissue samples from patients with cardiac hypertrophy, the researchers confirmed the results.
The results improve the understanding of cardiac hypertrophy and represent a promising start in this area. The search for new molecular targets for drugs used in the treatment of heart failure remains an area of intense research focus in the world.
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