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Chronic obstructive pulmonary disease is the third most common cause of death in the world after heart disease and stroke. One of the main triggers is smoking. Recent research shows that the two drugs available can help regenerate smoke-damaged lungs. Animal testing is ongoing for now.
- One of the most common causes of death in the world is chronic obstructive pulmonary disease (COPD), which obstructs the airflow in the lungs and leads to breathing problems.
- Doctors in the Netherlands have carried out a study showing that two drugs, used for other conditions, can help regenerate lungs damaged by cigarette smoke
- The effects of drugs have so far been tested in mice, but the expert, quoted by newscientist.com, believes that there is a good chance that they will be effective also in patients with COPD
- More important information can be found on the TvoiLokony home page
Chronic obstructive pulmonary disease is a condition that does not cause any specific symptoms for a long time. In patients suffering from COPD, airflow in the airways is obstructed and systematically deteriorates in the absence of appropriate treatment.
The disease of heavy smokers
The disease can be genetic or air pollution, but smoking is the most important contributing factor. Smokers account for 80-90 percent. sick. COPD is more common in men and in the elderly. The first symptom of the disease is the morning cough that persists for no specific reason (e.g. infection). As the disease progresses, there is a feeling of breathlessness and fatigue in activities that require physical exertion. Exercise is accompanied by coughing, loss of breath, and sometimes wheezing. In the advanced form of COPD, the patient experiences shortness of breath even at the slightest exertion.
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Two available drugs were tested
Researchers report that the two available drugs can help regenerate smoke-damaged lungs. After preliminary studies, they showed promise in restoring the regenerative capacity of mouse lung cells, suggesting they could be used to treat COPD in humans.
«The current problem with COPD is that we don’t have a way to prevent the disease from getting worse and lung function from worsening. We only have ways to treat the symptoms, for example with anti-inflammatory drugs or inhaled bronchodilators that relax the muscles of the lungs and widen the airways » — says Reinoud Gosens of the University of Groningen in the Netherlands, quoted by newscientist.com.
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COPD damages the so-called epithelial progenitor cells that normally regenerate the lining of the lungs. Previous efforts to treat this condition have focused mainly on invasive cell therapies such as stem cell implants, which are the source of progenitor cells. However, drug-based treatments could be easier to apply on a larger scale, either alone or in combination with other therapies.
Gosens and his colleagues analyzed data previously collected from the lung tissue of people with COPD and mice exposed to cigarette smoke, as well as data from healthy people and mice to find out which genes were more or less active in the diseased lung compared to healthy tissues.
Iloprost and misoprostol – hope for terminally ill?
This made it possible to identify two proteins in epithelial progenitor cells that contributed to the development of the disease and whose development may be limited by the use of two existing medicinal substances: iloprost, which is used to treat high blood pressure in the arteries of the lungs, and misoprostol, which is used to treat stomach ulcers.
To test these formulations, the team exposed the mice to cigarette smoke for four months, then used the drugs. Studies have shown that both drugs appear to fully restore the regenerative capacity of progenitor cells, which has decreased after exposure to cigarette smoke.
«Compared to other drugs that may support lung regeneration in animals, the big advantage of the drugs we identified is that they are already used to treat other conditions, so we know they are safe and equally effective» — said Gosens. He added, however, that patients with COPD are usually quite advanced in age, which certainly reduces the regenerative capacity of the lungs. Therefore, more research and the development of even better and more effective treatment models are needed.
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