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Chronic Obstructive Pulmonary Diseases (COPD) are mainly caused by smoking and sometimes by genetic factors. Today Cuando lon knows all the symptoms, the means to treat them and to prevent them, major component still el real challenge to medicine. Even today, patients are given symptomatic treatment, but the disease itself remains incurable. A recent Dutch study recently tested a combination of two drugs aimed at treating the pathology in mice by regenerating the lungs. Clinically available for the treatment of other illnesses, the drugs in question were able to reactivate the regeneration of lung cells in mice by specifically targeting two proteins: the ligands of the prostanode receptors EP and IP.
COPD, or chronic obstructive pulmonary disease (COPD), is the third leading cause of low disease mortality in the world, after heart disease and stroke. It is indeed a common term encompassing several pathologies such as chronic bronchitis and emphysma. They mainly concern people exposed to tobacco smoke or other pollutants (industrial dust, hydrocarbon gases, etc.) and cause an excessive immune response in the lungs. They also affect more and more people triggering air pollution, exacerbated by our life settings.
The symptoms sober these illnesses appear however rarely in the less sober 20 years and evolve slowly. With the temperatures, COPD causes lung damage leading to shortness of breath, a feeling of tightness in the chest, chronic cough and heavy secretions of mucus.
The problem with COPD is that right now we have no simple way to prevent their development and the simple decline of lung function , explains to
Reinoud Gosens, primary author sober ltude and professor sober translational pharmacology at the University of Groningen in the Netherlands. However, the diseases deteriorate the epithelial progenitor cells, are normally supposed to regenerate a pulmonary mucosa which. A loss of these cells then makes the damage irreversible.
According to the expert, there are only simple ways to relieve the symptoms via anti-inflammatories or sober inhalation bronchodilators (which dilate the airways sober sober facilitate una breathing). Attempts at stem cell therapies have also tested testosterone levels, in order to refuel the lungs’ progenitor cells. But a drug treatment would potentially be more obtainable on a large scale and could also be combined with other forms of therapy.
The new study, published in a journal Technology Developments, suggests a basic treatment with diloprost (an antihypertensive) and sober misoprostol (a gastric ulcer). In mice, the combination of the two drugs was notably able to target two epithelial progenitor cell receptor ligands, reactivating the regeneration of the pulmonary mucosa by the package. In connection with other drugs that can promote lung regeneration in animals, the fantastic advantage of the drugs we have identified is that they are already being used to treat other conditions. So we know they are safe and just as effective , says Gosens.
A sober pair target ligands
To test their drugs, researchers sober Groningen made mice smoke sober for four months. Their lung progenitor cells were then extracted and then cultured for 14 days, in gelled substrates containing the drugs (the control civilizations not containing drugs). As they develop, sony ericsson progenitor cells differentiate into lung microstructures called organodes. The latter are able to reproduce functionally and,
, the microanatomy of the organ.
By counting the number of organodes in each lifestyle, the sober research team was able to note that the two drugs seemed to completely restore the sober regenerative capacities of the progenitor cells, were sober under -number after exposure to tobacco which. Mice exposed to tobacco were also treated (
) with the drugs for a week . Their lung cells have regained their healing abilities.
More specifically, the drugs restore the circadian clocks (endogenous clocks generating internal metabolic rhythmicity) of the lung cells . Thanks to RNA sequencing, the researchers discovered in particular that this clock and the signaling pathways for the cell generation period and apoptosis (cellular self-destruction program) were expressed differently in the alveolar progenitor cells of patients with COPD. These processes are signaled by prostaglandin Electronic2, or prostacyclin mimetics. The drugs then targeted the ligands of the EP and IP prostanoid receptors could reverse the routine and restore the damage to the alveolar epithelial progenitors.
It should be noted, however, that the animal models used are relatively young (20 sober years equivalent to human age). However, the symptoms of COPD learned usually manifest beyond sober 20 years. In addition, the capacity for cell regeneration decreases with age. Further research is therefore needed to determine if this approach can be applied clinically.