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ARDS and DAD both involve acute damage to endothelial and alveolar epithelial cells, resulting in pulmonary edema. DAD has well-defined histologic stages, including cell exudation and hyaline membranes, followed by type II pneumocyte hyperplasia. More severe lesions progress to chronic interstitial fibrosis. ARDS and DAD have diverse causes in humans and animals, yet historically were viewed as universal pathways of tissue dysfunction irrespective of cause. Molecular data have suggested that ARDS has heterogeneous signatures in epithelial, endothelial, and inflammatory cells that can characterize the specific pathogenesis of individual cases and therefore support targeted treatment. The signatures are grouped into endotypes classified according to the mechanism of primary damage. The proposed ARDS endotypes are epithelial injury, endothelial injury, angiopathy, systemic inflammatory response, and local inflammatory response. We present the pathogeneses that form the foundation of the ARDS endotypes, including evidence from dogs and cats. Specific canine and feline causes of ARDS can be assigned to an ARDS endotype. For some etiologies, multiple endotypes are applicable, highlighting the need for increased resolution of the underpinning evidence to best support the accurate application of ARDS endotypes to clinical cases.<\/jats:p>","DOI":"10.1177\/10406387261418009","type":"journal-article","created":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T16:00:07Z","timestamp":1773244807000},"page":"695-710","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Diffuse alveolar damage, acute respiratory distress syndrome (ARDS), and non-cardiogenic pulmonary edema. 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