Targeting the Physiological Factors of Asthma
As a person who suffers from asthma, I can’t help but be
interested in any up-and-coming research involving how to prevent or treat the
disease. I have always had to carry a rescue inhaler on
my person in case of an unexpected attack, which can be a pain at times. While
there are medications out there today that treat the symptoms, like corticosteroids
(for inflammation), it would be nice to see a treatment developed that targets
the cause and can help improve lung function in individuals like me. By understanding the physiology behind asthma
attacks, we are getting closer and closer to seeing improved treatments become
reality.
In papers recently published by the Proceedings of the
National Academy of the Sciences (PNAS), scientists from UCSF, Johns Hopkins
University, and Duke University demonstrated that TMEM16A, a specific
calcium-activated chloride channel, could hold clues in reducing some of the
processes that contribute to the severity of asthma.
As it turns out, humans normally have relatively few
mucus-producing cells lining the tubes to the lungs, but asthma sufferers have
elevated numbers of these cells, as well as a hyperplasia of airway smooth
muscle cells (ASM) in this region.
Together these factors are what generate the two most common symptoms of
asthma: mucus hypersecretion and ASM hyperresponsiveness.
Studies have shown that the transmembrane protein known as
TMEM16A is a calcium-activated chloride channel (CaCC) which holds an increased
expression in asthmatics. In other
words, TMEM16A is activated specifically by an increase in intracellular
calcium and plays a role in these unwanted processes. Because the molecular identity of this protein
was unknown until recently, research is still in the early stages. This means that the development of
CaCC-targeted therapies at this point is limited; however, as research
progresses, it may prove beneficial in the development of better strategies for
managing asthma.
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