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Review Article Open Access
People living in plains often travel to high altitude regions for trekking, expedition, pilgrimage and deployment. Hypobaric hypoxia is one of the major challenges at high altitude. Since the people living at plains are not accustomed to oxygen scarcity prevailing at high altitude (HA), they often suffer from various high altitude maladies such as acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE), high-altitude cerebral edema (HACE) or chronic mountain sickness (CMS). Amongst these, HAPE and HACE are the life threatening complications, and it has been evident from several studies that some individuals are genetically more susceptible to high altitude maladies than others. The incidences of these high-altitude diseases are variable and difficult to predict. The occurrences of these maladies also depend on the rate of ascent and the altitude attained. Study of genetic variations amongst individuals can explain the inter-individual variations in susceptibility towards hypoxia and HAPE. The rennin-angiotensin-aldosterone system (RAAS) pathway, which is a major endocrine system, plays a key role in maintaining physiological homeostasis of blood pressure and electrolyte balance in the body. Since HAPE is commonly associated with pulmonary hypertension and elevated capillary pressure, the genetic variations in RAAS pathway could be playing a significant role in susceptibility of an individual towards HAPE. This brief review focuses on the functional relevance of polymorphisms in genes of RAAS pathway as revealed in several genetic studies, in susceptibility towards HAPE.
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Author(s): Swati Srivastava Seema Dwivedi
RAAS, HAPE, High Altitude, Polymorphism, Molecular Biology & Endocrinology, Endocrinology, Thyroid Endocrinology