2024-01-29 10:15:46
Pulmonary hypertension is characterized by high pressure in the arteries that go to the lungs, which causes the heart to continually overexert itself.
It affects between 15 and 50 people per million inhabitants. In Spain, a prevalence of 1.6 cases and an incidence (new cases diagnosed per year) of 0.3 per 100,000 inhabitants are calculated. It is a rare disease.
People who suffer from pulmonary hypertension often face symptoms that significantly reduce their quality of life: respiratory distress, dizziness and fainting, and a transplant may even be necessary to prevent the patient’s death.
There are several risk factors that can contribute to its development such as smoking, being overweight, the existence of previous diseases, genetic predisposition or being exposed to low levels of oxygen in high altitude areas.
To date, existing therapies target the lung, seeking to reduce blood pressure. However, these strategies do not seem to improve cardiac function, making heart failure the main cause of death in these patients.
In a new study, COPD (Chronic Obstructive Pulmonary Disease) patients examined have been found to have higher levels of the mitochondrial protein called MCJ. And a possible therapeutic target against pulmonary hypertension has been found.
The study is the work of a team led by Dr. Guadalupe Sabio at the National Center for Cardiovascular Research (CNIC), a center dependent on the Carlos III Health Institute (ISCIII), an organization attached to the Ministry of Science, Innovation and Universities of Spain.
Researcher Ayelén M. Santamans, first author of the study, observed that the same situation described occurred in mice exposed to low levels of oxygen and in pigs with some type of heart damage, so, says Santamans, “these results suggested that the protein MCJ might be involved in pulmonary hypertension. The lack of cardiospecific therapies motivated us to move forward in that direction.”
Ayelén M. Santamans and Guadalupe Sabio. (Photo: CNIC)
Their research demonstrates that modulating the levels of the mitochondrial protein MCJ in the heart can preserve cardiac function despite lung damage.
This protection, the researchers explain, is caused by the activation of a signaling pathway essential for adaptation to low levels of oxygen, which prepares the heart so that it can function correctly in the face of a lack of oxygen.
These scientists conclude that these findings could open new doors for possible therapeutic interventions against pulmonary hypertension since they offer the first target capable of saving cardiac function in this lethal disease.
The study is titled “MCJ: A mitochondrial target for cardiac intervention in pulmonary hypertension.” And it has been published in the academic journal Science Advances. (Source: CNIC / ISCIII)
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