A recently studied protein called GDF 11 could help prevent —or even reverse— the lung-damage caused by chronic obstructive pulmonary disease, or COPD, say scientists, who urge for more research into this age-defying “fountain of youth” as a COPD treatment.
COPD, an umbrella term describing progressive lung disease (bronchitis, emphysema and asthma are all variants of COPD), is most commonly associated with cigarette smoking, where difficulty breathing, coughing and mucus production are a result of damage to the lungs caused by smoking.
Yet even though smoking rates have declined in the developed world over recent decades (they continue to rise, unfortunately, in the developing world), health care workers are still seeing dramatic increases in the number of patients with COPD. In fact, cases of COPD are expected to double over the next 20 years. The problem, it turns out, is that even with healthier lungs, we’re all aging.
“Most industrialized countries of the world are getting older and, unquestionably, COPD is an age-related disorder,” say Dr. Ma’en Obeidat of the University of British Columbia’s Centre for Heart Lung Innovation and Dr. Don Sin of UBC’s Department of Medicine, in a recent editorial for the journal Thorax. “Whereas COPD is almost unheard of in individuals less than 40 years of age (even among heavy smokers), one in ten lifetime never-smokers and one in three smokers develop COPD by age 75.”
Thus, one potential avenue for addressing COPD involves looking at factors that influence the physiological aging process. And on that front, there is no better candidate for investigation than the age-related protein called GDF 11, say Obeidat and Sin, who state that recent research into GDF 11 suggests that it could help with treatment of COPD.
Growth differentiation factor 11 plays a role in cell signalling and tissue growth, and research has shown that it has surprising anti-aging effects. One study found that it acts as a blood circulating factor to actually reverse the heart muscle thickening process known as cardiac hypertrophy in mice. Others have shown that GDF 11 can reverse age-related dysfunction in skeletal muscle and improve blood flow and increase cell growth in the brain.
Now, a new study from researchers at Tohoku University Graduate School of Medicine in Sendai, Japan, have found a significant connection between GDF 11 and CPOD, concluding that blood plasma levels of GDF 11 in patients with COPD were decreased in comparison to those
without the disease.
Researchers took lung tissue from patients with COPD and treated it with GDF 11, finding the protein helped suppress the process of senescence, or cell degeneration, a result which was then also replicated in lab mice.
“The findings are exciting and novel and may represent a new therapeutical and biomarker target to modulate COPD and establish cellular senescence as an important player in the pathogenesis of COPD,” say Obeidat and Sin, who argue that more research is needed on the GDF 11 and its role in COPD.
In 2014, GDF 11 was named a runner-up for science breakthrough of the year in the journal Science.
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