{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T22:45:05Z","timestamp":1788993905840,"version":"build-2803163510"},"reference-count":70,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T00:00:00Z","timestamp":1769126400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T00:00:00Z","timestamp":1769126400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>Absract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Purpose<\/jats:title>\n                    <jats:p>\n                      Bronchopulmonary dysplasia (BPD) affects premature newborns, particularly those receiving supplemental oxygen therapy. Exposure of underdeveloped lungs to oxygen levels higher than the intrauterine environment causes oxidative stress, impairing alveolarisation, vascularisation and causing fibrosis. The \u03b2\n                      <jats:sub>3<\/jats:sub>\n                      \u2010adrenoceptor could represent a promising target for BPD treatment because of its oxygen\u2010dependent regulation, ability to reduce oxidative stress and protection against intestinal hyperoxia\u2010induced damage.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      In this study, neonatal rat pups were reared under hyperoxia for 2\u2009weeks to induce a BPD\u2010like disease and treated with the \u03b2\n                      <jats:sub>3<\/jats:sub>\n                      \u2010adrenoceptor agonist BRL37344 (1, 3 or 6\u2009mg\u2009kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Through oxidative stress, hyperoxia decreases pulmonary volume, impairs alveolarisation and vascularisation, and causes fibrosis and type II pneumocyte hyperplasia, thereby reducing survival rates. BRL37344 at 3\u2009mg\u2009kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      counteracted these alterations, doubling survival rates.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      Our findings demonstrate a new role for \u03b2\n                      <jats:sub>3<\/jats:sub>\n                      \u2010adrenoceptors in protecting the lungs from hyperoxic injury, suggesting its pharmacological activation as a strategy for treating Bronchopulmonary dysplasia of prematurity and, possibly, other lung fibrosis\u2010related disorders.\n                    <\/jats:p>\n                  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