Smoking Causes Lungs to Lose Their Ability to Heal
Cigarette smoke has the potential to block self-healing processes in the lungs by eroding molecules responsible for the renewal of lung cells and certain proteins essential for breathing, consequently leading to chronic obstructive pulmonary disease (COPD), claimed a study.
Representative image. (Photo Credit: Reuters)
Are you a chain smoker? Beware. Cigarette smoke has the potential to block self-healing processes in the lungs by eroding molecules responsible for the renewal of lung cells and certain proteins essential for breathing, consequently leading to chronic obstructive pulmonary disease (COPD), claimed a study.
In patients with COPD -- manifested mainly through cough, bronchitis and breathing difficulties -- the lung's natural self-healing, no longer takes place.
"In healthy patients, the so-called WNT/beta-catenin signalling pathway is responsible for the lung's homeostasis. Until now, it was not clear why it was silenced in patients with COPD," said Melanie Konigshoff from Helmholtz Zentrum Munchen -- German Research Centre for Environmental Health.
The new study revealed that one of the Frizzled molecules -- Frizzled 4, when exposed to smoke -- plays an important role in halting lung's natural self-healing process.
In the lung tissue of COPD patients, and especially that of smokers, there were significantly fewer Frizzled 4 receptors than in non-smokers, the researchers said.
"Frizzled 4 is a receptor molecule that sits on the surface of lung cells, where it regulates their self-renewal via WNT/beta-catenin," explained Wioletta Skronska-Wasek, doctoral student at Helmholtz Zentrum Munchen.
"However if the cells are exposed to cigarette smoke, Frizzled 4 disappears from the surface and cell growth comes to a halt," Skronska-Wasek added in the paper, reported in the American Journal of Respiratory and Critical Care Medicine.
Inhibition of Frizzled 4 signalling on the cells led to decreased WNT/beta-catenin activity and consequently to reduced wound healing and repair capacity, the researchers noted.
On the other hand, "the activation of the Frizzled 4 receptor can restore the WNT/beta-catenin signalling pathway and consequently lead to repair in the lung," Konigshoff said.
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