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Thus, within the age range examined, this mouse model does not reproduce the cardiomyopathic phenotype associated with the CRYABR120G mutation in patients. These findings underscore the importance of validating genetic mouse models, as they may incompletely reflect the pathophysiological mechanisms and disease progression observed in humans.\n                  <\/jats:p>","DOI":"10.1152\/ajpheart.00364.2026","type":"journal-article","created":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T12:52:22Z","timestamp":1783428742000},"page":"H588-H596","update-policy":"https:\/\/doi.org\/10.1152\/aps-crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["The R120G knock-in mutation in \u03b1B-crystallin is insufficient to induce cardiomyopathy in mice"],"prefix":"10.1152","volume":"331","author":[{"given":"Justin M.","family":"Quiles","sequence":"first","affiliation":[{"name":"University of California San Diego","place":["United 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