News: Johns Hopkins study probes root causes of pulmonary hypertension

CDI Strategies - Volume 12, Issue 13

Johns Hopkins researchers say they’ve made a breakthrough in understanding the underlying biology behind pulmonary hypertension, according to the Johns Hopkins release.

The researchers conducted experiments in endothelial cells and discovered that a protein protects the cells from damage in the event of severe conditions such as oxygen deprivation that may lead to pulmonary hypertension.

During a state of reduced oxygen, the protein levels can drop, which causes a chain reaction that likely contributes to blood vessel damage and the progression of pulmonary hypertension, the release says. 

In proof of concept studies, the researchers were able to genetically alter cells grown in a dish, causing them to have increased protein expression and reverse the damage, restoring the cells to normal function after low oxygen levels.

“The findings potentially advance the search for drugs that not only control pulmonary hypertension but also may reverse the disease or cure it,” said Lewis Romer, MD, senior co-author of the study and a professor of anesthesiology and critical care medicine, cell biology, biomedical engineering and pediatrics at the Johns Hopkins University School of Medicine.

Pulmonary hypertension can currently be managed through medications that maximize blood flow through the lungs or, in severe cases, a heart or lung transplant. The disease accounts for an estimated $4.9 to $5.8 billion in annual healthcare spending worldwide, according to the release. Untreated, the disease presents roughly 50% mortality within two to five years of the diagnosis, Romer said, “so it’s very important for the medical community to get a better handle on what’s going on with the underlying disease.” 

Editor’s note: To read the full release from Johns Hopkins, click here. To read about recent advice from AHA Coding Clinic on pulmonary hypertension, click here

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