{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T20:59:18Z","timestamp":1788209958041,"version":"build-2803163510"},"reference-count":67,"publisher":"Portland Press Ltd.","issue":"14","license":[{"start":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T00:00:00Z","timestamp":1751328000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,7,31]]},"abstract":"<jats:p>Angiotensin II AT2 receptor (AT2R) activation leads to significant anti-fibrotic and anti-inflammatory effects in diseased organs, which has led to clinical trial evaluation of the AT2R agonist, Compound 21 (C21), as a treatment for idiopathic pulmonary fibrosis (IPF). In this study, the anti-fibrotic effects of a more selective AT2R ligand, \u03b2-Pro7 angiotensin III (\u03b2-Pro7 Ang III), with &amp;gt;20,000-fold affinity for the AT2R over the AT1R, were compared with that of C21 or the currently used IPF medication, pirfenidone, in mice with bleomycin (BLM)-induced pulmonary fibrosis. Adult female BALB\/c mice received a double intranasal instillation of BLM (20 mg\/kg\/day) seven days apart and were maintained until day 35, while control mice were instilled with saline (SAL) seven days apart and maintained for the same time period. Sub-groups of BLM-injured mice were then treated on day 28 with vehicle (SAL), C21 (0.3 mg\/kg\/day) or \u03b2-Pro7 Ang III (0.1 mg\/kg\/day) via seven-day subcutaneously implanted osmotic minipumps, or daily from days 28 to 35 via orally administered pirfenidone (100 mg\/kg\/day). At day-35 post-injury, measures of lung fibrosis and compliance were evaluated. Compared with their SAL-instilled counterparts, SAL-treated BLM-injured mice presented with a significantly increased lung Ashcroft score, Masson\u2019s trichrome-stained and second harmonics generation-measured fibrosis, myofibroblast accumulation, and TGF-\u03b21 expression, but reduced lung dynamic compliance at day-35 post-injury. While all treatments evaluated attenuated the BLM-induced lung myofibroblast accumulation and TGF-\u03b21 expression, AT2R stimulation, but not pirfenidone, attenuated lung collagen deposition after seven days. \u03b2-Pro7 Ang III also significantly restored lung compliance and promoted collagen-degrading matrix metalloproteinase-2 activity. These findings highlighted the therapeutic value of selectively targeting the AT2R for treating IPF.<\/jats:p>","DOI":"10.1042\/cs20245138","type":"journal-article","created":{"date-parts":[[2025,7,1]],"date-time":"2025-07-01T05:54:33Z","timestamp":1751349273000},"page":"809-824","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["The novel AT2 receptor ligand, \u03b2-Pro7 Ang III, induces equivalent anti-fibrotic effects to Compound 21 but broader anti-fibrotic effects than pirfenidone in mice with bleomycin-induced pulmonary fibrosis"],"prefix":"10.1042","volume":"139","author":[{"given":"Simon G.","family":"Royce","sequence":"first","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cem","family":"Erdem","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"WeiYi","family":"Mao","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Wang","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark P.","family":"Del Borgo","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6515-0435","authenticated-orcid":false,"given":"Robert E.","family":"Widdop","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0295-4214","authenticated-orcid":false,"given":"Chrishan S.","family":"Samuel","sequence":"additional","affiliation":[{"name":"Cardiovascular Disease Program, Monash Biomedicine Discovery Institute and Department of Pharmacology, Clayton, Victoria, 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2025,7,31]]},"reference":[{"key":"2025073112162330600_CS-2024-5138C1","doi-asserted-by":"crossref","first-page":"250","DOI":"10.1016\/j.pharmthera.2013.10.008","article-title":"Novel therapeutic strategies for lung disorders associated with airway remodelling and fibrosis","volume":"141","author":"Royce","year":"2014","journal-title":"Pharmacol. 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