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Smoking hampers lung`s ability to heal
Are you a chain smoker? If yes, then avoid or quit smoking as it can cause lungs to lose their ability to heal.
London: Are you a chain smoker? If yes, then avoid or quit smoking as it can cause lungs to lose their ability to heal.
A new study has claimed that 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).
In patients with COPD manifested mainly through cough, bronchitis and breathing difficulties, the lung's natural self-healing, no longer takes place.
Melanie Konigshoff from Helmholtz Zentrum Munchen -- German Research Centre for Environmental Health said, "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".
The new findings has revealed that one of the Frizzled molecules called 'Frizzled 4' when exposed to smoke plays an important role in halting lung's natural self-healing process.
Researchers said that in the lung tissue of COPD patients, and especially that of smokers, there were significantly fewer Frizzled 4 receptors than in non-smokers.
"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.
(With IANS inputs)