{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T21:25:42Z","timestamp":1790198742545,"version":"4.1.0"},"reference-count":64,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2026,1,2]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>ADAR1 (adenosine deaminase acting on RNA 1) catalyzes the conversion of adenosine to inosine in double stranded RNAs (dsRNAs), which is critical to prevent autoinflammatory responses mediated by activation of the type I IFN (interferon) signaling. We define the role of ADAR1-dependent RNA editing in IFN\u03b2 activation in pulmonary arterial smooth muscle cells (PASMCs) from idiopathic pulmonary arterial hypertension (IPAH), a devastating disease leading to right heart failure and death.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      RNA editing levels were analyzed in PASMCs from IPAH patients versus healthy controls. A conditional transgenic mouse model,\n                      <jats:italic toggle=\"yes\">Adar1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">SMC<\/jats:italic>\n                        -\n                      <\/jats:sup>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">KO<\/jats:italic>\n                      <\/jats:sup>\n                      , was generated by knocking out\n                      <jats:italic toggle=\"yes\">Adar1<\/jats:italic>\n                      selectively in Sma (smooth muscle actin)\u2013expressing cells, followed by 3 weeks of hypoxic exposure to induce pulmonary hypertension (PH).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      PASMCs from patients with IPAH displayed decreased levels of ADAR1 mRNA and isoform p150 protein, accompanied by accumulated dsRNA compared with healthy PASMCs. ADAR1 knockdown in PASMCs upregulated MDA5 (melanoma differentiation-associated protein 5), PKR (protein kinase R), IFN\u03b2, and IFN-stimulated genes. Compared with controls in vivo, hypoxic\n                      <jats:italic toggle=\"yes\">Adar1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">SMC<\/jats:italic>\n                      <\/jats:sup>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">-KO<\/jats:italic>\n                      <\/jats:sup>\n                      mice developed severe PH, as evidenced by excessive vascular remodeling in distal arterioles and increased endothelium leakage, resulting in elevated right ventricular systolic pressure and right ventricular hypertrophy. Mechanistically, Ifn\u03b2 signaling in\n                      <jats:italic toggle=\"yes\">Adar1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">SMC-KO<\/jats:italic>\n                      <\/jats:sup>\n                      induced the recruitment of macrophages, enhancing pulmonary artery muscularization. Pharmacological treatment with Pkr-relevant inhibitor 2BAct decreased Ifn\u03b2 and macrophages, thus attenuating pulmonary hypertension (PH) in hypoxic\n                      <jats:italic toggle=\"yes\">Adar1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">SMC-KO<\/jats:italic>\n                      <\/jats:sup>\n                      mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Our study describes a fundamental molecular mechanism underlying the progression of PH. We highlight the detrimental role of innate immune responses, where smooth muscle cell and context-specific RNA editing, along with the sensing of dsRNA, mediate disease progression and excessive vascular remodeling. This finding suggests that targeting PKR could be the new therapeutic strategy for treating pulmonary arterial hypertension.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circresaha.125.326235","type":"journal-article","created":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T09:00:13Z","timestamp":1761123613000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":9,"title":["Deficiency of Smooth Muscle Adar1 Exacerbates Vascular Remodeling and Pulmonary Hypertension"],"prefix":"10.1161","volume":"138","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-1804-571X","authenticated-orcid":true,"given":"Yunhye","family":"Kim","sequence":"first","affiliation":[{"name":"Division of Pulmonary Medicine, Boston Children\u2019s Hospital, Harvard Medical School, MA (Y.K., H.K., T.K., Y. Li, Y.H., B.A.R., K.Y.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8245-5348","authenticated-orcid":true,"given":"Giovanni","family":"Maroli","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health, Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany (G.M., C.V., C.R., S.S.P.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4291-1788","authenticated-orcid":true,"given":"Chen-Shan Chen","family":"Woodcock","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Center for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute, University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center, PA (C.-S.C.W., M.L., C.K., T.A., Y.T., Y.-Y.T., T.V.K., R.S., S.Y.C.)."},{"name":"Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, CO (C.-S.C.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7193-0278","authenticated-orcid":true,"given":"Hyunbum","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Medicine, Boston Children\u2019s Hospital, Harvard Medical School, MA (Y.K., H.K., T.K., Y. Li, Y.H., B.A.R., K.Y.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7110-127X","authenticated-orcid":true,"given":"Yu","family":"Liu","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Medicine, Boston Children\u2019s Hospital, Harvard Medical School, MA (Y.K., H.K., T.K., Y. Li, Y.H., B.A.R., K.Y.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tim","family":"Klouda","sequence":"additional","affiliation":[{"name":"Division of Pulmonary Medicine, Boston Children\u2019s Hospital, Harvard Medical School, MA (Y.K., H.K., T.K., Y. Li, Y.H., B.A.R., K.Y.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4504-558X","authenticated-orcid":true,"given":"Yan","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Medicine, Stanford University, CA (Y. 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