{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T04:46:50Z","timestamp":1782708410984,"version":"3.54.5"},"reference-count":49,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T00:00:00Z","timestamp":1774483200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T00:00:00Z","timestamp":1774483200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81860077"],"award-info":[{"award-number":["81860077"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>\n                      The aim of this study is to determine whether Angiotensin\u2010(1\u20137) [Ang\u2010(1\u20137)] alleviates isoproterenol (ISO)\u2013induced cardiac hypertrophy by suppressing excessive autophagy and apoptosis through coordinated Mas receptor (MasR) and angiotensin II type\u20102 receptor (AT\n                      <jats:sub>2<\/jats:sub>\n                      R) signaling, and to elucidate the underlying mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      ISO\u2010induced hypertrophy was established in mice and assessed by echocardiography, histology, and hypertrophic markers. H9c2 cardiomyocytes were exposed to ISO and treated separately with A\u2010779 (MasR antagonist), PD123319 (AT\n                      <jats:sub>2<\/jats:sub>\n                      R antagonist), and a combination of both receptor antagonists. Receptor interplay was examined using pharmacological blockade and co\u2010immunoprecipitation. Autophagy and apoptosis were evaluated by transmission electron microscopy and TUNEL.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ang\u2010(1\u20137) attenuated ventricular dysfunction, myocardial enlargement, and upregulation of hypertrophic markers in mice with ISO\u2010induced hypertrophy. Pharmacological inhibition with A\u2010779 and PD123319 revealed that Ang\u2010(1\u20137) actions require reciprocal regulation between MasR and AT\n                      <jats:sub>2<\/jats:sub>\n                      R. Both receptors synergistically contributed to the anti\u2010apoptotic effect, while the anti\u2010autophagic response was mediated predominantly by MasR. Transmission electron microscopy and TUNEL staining confirmed that Ang\u2010(1\u20137) treatment alleviated excessive autophagy and apoptosis in cardiomyocytes. Furthermore, experiments with dual receptor antagonists and co\u2010immunoprecipitation showed an interaction between MasR and AT\n                      <jats:sub>2<\/jats:sub>\n                      R, supporting their coordinated signaling role in cardiac protection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Ang\u2010(1\u20137) ameliorates ISO\u2010induced cardiac hypertrophy by suppressing excessive autophagy and apoptosis via synergistic MasR\u2013AT\n                      <jats:sub>2<\/jats:sub>\n                      R signaling. Receptor crosstalk may represent a therapeutic entry point for pathological hypertrophy.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.70200","type":"journal-article","created":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T21:09:02Z","timestamp":1774559342000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Angiotensin\u2010(1\u20137) Alleviates Isoproterenol\u2010Induced Cardiac Hypertrophy by Suppressing Autophagy and Apoptosis Through the Synergistic Action of Mas Receptor and Angiotensin\n                    <scp>II<\/scp>\n                    Type 2 Receptor"],"prefix":"10.1111","volume":"242","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-3629-4303","authenticated-orcid":false,"given":"Xiaomei","family":"Wang","sequence":"first","affiliation":[{"name":"College of Pharmacy Yanbian University  Yanji 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