Growth of heart tissue is beneficial when the human body is young and developing. Heart expansion that occurs after the heart is fully grown? Not so much.
A study recently published in
Nucleic Acids Research studied the role of DPF and DPF3a proteins in cases of cardiac hypertrophy, an irregular enlargement of heart muscle that is caused by cardiac stress and results in more cardiac stress (
Nature). When DPF3a is activated at a young age, heart muscle develops normally and healthily. When DPF3a is activated during adulthood, the heart expands dangerously to the point where pumping blood is difficult and tissues do not receive the nutrients and oxygen they need to function.
The recently published study, conducted by researchers from the Experimental and Clinical Research Center, Max Planck Institute for Molecular Genetics, and Harvard Medical School, identified DPF3a protein’s role in binding a transcriptional repressor after phosphorylation-related activation. By binding a transcriptional repressor protein, the protein was unable to inhibit certain genes like normal. The genes that the specific transcriptional repressor protein inhibits promote early cardiac development. When DPF3a binds during adulthood, the heart cells grow and make a healthy-sized adult many sizes too big.
Understanding this pathway is key toward preventing and treating various cardiovascular conditions like stroke, high blood pressure, and heart attack.
“Our research represents a promising start in this area,” said Professor Dr. Silke Rickert-Sperling from the Experimental and Clinical Research center.
DPF3a is not a “bad” protein; it is much needed when the body is first developing. However, the body is prone to making harmful mistakes. Preventing or fixing these mistakes is an important step toward reducing the risk of disease.
Source:
Charité - Universitätsmedizin Berlin
