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Abstract Introduction: High-altitude pulmonary edema (HAPE) is a severe complication of rapid exposure to high-altitude hypoxia, but its molecular mechanisms remain incompletely understood. This study aimed to characterize lung proteomic alterations in HAPE and identify candidate proteins associated with its pathophysiological processes. Methods: Male Wistar rats were randomly allocated to control and HAPE model groups (n = 20/group).
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