Smoking harms almost every organ of your body and causes 87% of lung cancer deaths. Smoking tobacco is amongst the leading causes of many other diseases such as heart attack, COPD, erectile dysfunction, and birth defects. It has become a most popular form of drug abuse. Smoking is dated as early as 500 BC, and today, approximately 1.1 billion people, and up to 1/3 of the adult population engage in smoking. According to a new study, the smoke emerged from cigarettes can block the self healing process in lungs and can consequently lead to chronic obstructive pulmonary disease.This finding has been reported in the American Journal of Respiratory and Critical Care Medicine by the researchers at the Helmholtz Zentrum Munchen, partner in the German Centre for Lung Research (DZL), and their international colleagues.
The typical symptoms of COPD include cough, bronchitis and breathing difficulties. Though exact figures are not available, the estimates are that 10 to 12% of adults over 40 years of age in Germany suffer from the disease. Experts have estimated the national economic costs of the disease at almost six billion euros annually. Scientists around the world are making efforts to discover how the disease is developed and what biological adjustments can be made to stop it.
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One of the approaches involved the lung's natural self-healing, which no longer takes place in COPD. "In healthy patients, the so-called WNT/beta-catenin signaling pathway is responsible for the lung's homeostasis. Until now, it was not clear why it was silenced in patients with COPD," said Dr Melanie Konigshoff, head of the Lung Repair and Regeneration (LRR) Research Unit of the Comprehensive Pneumology Center (CPC) at Helmholtz Zentrum Munchen. She and her team spent the last few years tackling this question in the framework of an ERC starting Grant and discovered that one of the Frizzled molecules - Frizzled 4 - played an important role.
"Frizzled 4 is a receptor molecule that sits on the surface of lung cells, where it regulates their self-renewal via WNT/beta-catenin," said author Wioletta Skronska-Wasek, doctoral candidate at the LRR. "However if the cells are exposed to cigarette smoke, Frizzled 4 disappears from the surface and cell growth comes to a halt."
The current study's starting point was the team's observation that in the lung tissue of COPD patients, and especially that of smokers, there were remarkable low Frizzled 4 receptors than in non-smokers. "In the next step, we were able to prove in cell culture and model systems that inhibition of Frizzled 4 signalling on the cells led to decreased WNT/beta-catenin activity and consequently to reduced wound healing and repair capacity," said Dr Alinder Yildirim, an expert on the effects of cigarette smoke in the lung. The authors additionally recognized that without the receptor, there was a loss of certain proteins that are important for the structure of lung tissue (including elastin, fibulin and IGF1) and the lung's elasticity, allowing patients to breathe.
To confirm their results, the scientists artificially enhanced the Frizzled 4 levels in a cell culture test to stimulate its production. The increase in Frizzled 4 level reactivated the blocked repair process and led to the production of many of the previously reduced proteins.
"The activation of the Frizzled 4 receptor can restore the WNT/beta-catenin signalling pathway and consequently lead to repair in the lung," said Melanie Konigshoff. This is an exciting starting point for further research which might develop new therapies for COPD patients.