Targeted treatment for respiratory conditions, especially sleep apnea, are possible with the discovery of a breathing molecule found in new research out of the University of Warwick.
The name of the molecule is Connexin26 (Cx26). It identifies CO2 levels in the blood and then activates the breathing mechanisms that release it, which means it has evolved specifically for this purpose.
This new research could lead to better treatment options for respiratory conditions and even deafness because physicians will be able to target the problem more accurately.
A professor at the School of Life Sciences by the name of Nicholas Dale is the person who made the discovery of Connexin26 (Cx26). He identified it as the key molecule that reacts to CO2 levels, which then causes the body to activate the muscles necessary for breathing.
The discovered molecules are responsible for alerting the body when CO2 levels reach a certain point in the bloodstream and need to be excreted through exhalation, as well as take in oxygen for replenishment with inhalation. This is the vital process of preserving life, and we now have an identified molecule that activates that involuntary process of breathing, allowing blood to flow to the brain.
If this molecule were to malfunction or stop working, our bodies would fill with CO2 and breathing would become exceedingly difficult or near to impossible. Furthermore, high CO2 levels can be toxic to the human body.
The Cx26 molecule can mutate, and there are a number of serious medical conditions that are associated with this mutation, including congenital deafness and respiratory diseases. Cx26 mutations are associated with vision impairment and skin syndromes as well. Those who have these mutations are at increased risk of sleep apnea because properly Cx26 molecular function is directly associated with comfortable breathing.
Professor Dale notes that identification of these molecular mutations will allow scientists to work with them and discover ways to restore the molecule to normal function, which could also include targeted treatment options more personalized in nature, thereby improving patient experience and quality of life.
Each being on earth has a different tolerance level to CO2 in their bloodstream. This group looked further at this theory to see if the Cx26 properties would match in different animals. They analyzed birds because of their high-altitude flying and their ability to tolerate higher levels of CO2. Furthermore, humans were similar to rats in CO2 tolerance, and mole rates (who live underground) had extremely high tolerance to CO2.
This team of researchers discovered that the binding properties of CO2 correlated with the sensitivity levels in each animal examined. Natural selection in our evolutionary scale has modified the CO2 binding properties in the Cx26 molecule, leading researchers to believe that the molecule is universally important to warm-blooded animals when it comes to detecting CO2 levels. This finding could certainly add weight to research in sleep apnea treatments.
Regarding the findings, Professor Dale notes that these important molecules show universal function in the physiological sense, which evolution has continually shaped over time. This fact was shown in these findings, he notes, because CO2 binding characteristics in the Cx26 molecule are necessary for us to breathe and survive. This will likely help scientists discover better treatment options for people with respiratory illnesses, especially sleep apnea.
Professor Dale published ‘Evolutionary Adaptation of the Sensitivity of Connexin26 Hemichannels to CO2’ in Proceedings of the Royal Society B.
Rachael Herman is a professional writer with an extensive background in medical writing, research, and language development. Her hobbies include reading, traveling, and cooking.