A Role for Calcineurin Signaling in Hypoxia-Influenced Cardiac Growth
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In 1925, Dr Carlos Monge presented to the National Academy of Medicine in Lima, Peru, his observations of a new disease. His patient had bluish skin, dizziness, and confusion when working at high altitudes, but symptoms were ameliorated once the patient returned to the coast.1 In a storied and impactful career, Monge went on to study the physiological differences between sufferers of Monge’s disease, those who were able to acclimatize to the altitude, and finally those who thrived in the low oxygen conditions.2 Today, we now know this condition as chronic mountain sickness (CMS). Caused by exposure to low oxygen conditions, CMS affects a significant proportion of high-altitude populations and can lead to pulmonary hypertension, cardiac hypertrophy, and eventual heart failure.3
See Article by Zarndt and Walls et al
Today, CMS still afflicts a large number of individuals, including a striking one sixth of residents of Cerro de Pasco in Peru,4 designating CMS as a significant medical challenge in many high-altitude populations. Understanding the mechanisms by which hypertension and cardiac hypertrophy occur as a result of hypoxia is important not only …