{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T16:36:53Z","timestamp":1793205413806,"version":"4.5.0"},"reference-count":34,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T00:00:00Z","timestamp":1786320000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T00:00:00Z","timestamp":1786320000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100005089","name":"Natural Science Foundation of Beijing Municipality","doi-asserted-by":"publisher","award":["7262112"],"award-info":[{"award-number":["7262112"]}],"id":[{"id":"10.13039\/501100005089","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Anim Models and Exp Med"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hypoxic pulmonary hypertension (HPH) is a progressive chronic disorder characterized by elevated mean pulmonary arterial pressure. It severely impairs right ventricular function and ultimately causes right ventricular failure. Clarifying the complex pathogenesis of HPH remains a critical challenge.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Rat HPH models were established by exposure to a hypobaric hypoxia chamber for 4 consecutive weeks. Lung tissues were harvested for RNA sequencing. The Coding\u2010Non\u2010Coding Index (CNCI) and Coding Potential Calculator (CPC) were used to construct a competing endogenous RNA (ceRNA) network. Pulmonary artery endothelial cells were transfected with modified\n                      <jats:italic>lncRNA\u201092467<\/jats:italic>\n                      or\n                      <jats:italic>miR\u2010205\u20105p<\/jats:italic>\n                      to assess their regulatory functions. Finally, mice were injected with AAV\u2010Control or AAV\u2010\n                      <jats:italic>PTPRM<\/jats:italic>\n                      shRNA (2.5\u2009\u00d7\u200910\n                      <jats:sup>11<\/jats:sup>\n                      v.g.\/mL per mouse). Hemodynamic and echocardiographic analyses were performed to evaluate the in\u00a0vivo role of\n                      <jats:italic>PTPRM<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified that\n                      <jats:italic>lncRNA\u201092467<\/jats:italic>\n                      functions as a competing endogenous RNA (ceRNA) by competitively binding to\n                      <jats:italic>miR\u2010205\u20105p<\/jats:italic>\n                      , thereby upregulating its target gene\n                      <jats:italic>PTPRM<\/jats:italic>\n                      . Knockdown of\n                      <jats:italic>lncRNA\u201092467<\/jats:italic>\n                      significantly promoted pulmonary artery endothelial cell proliferation and migration. These effects were abolished by a\n                      <jats:italic>miR\u2010205\u20105p<\/jats:italic>\n                      inhibitor, which also restored\n                      <jats:italic>PTPRM<\/jats:italic>\n                      expression. Functional assays confirmed that\n                      <jats:italic>miR\u2010205\u20105p<\/jats:italic>\n                      enhanced cell proliferation and migration while inhibiting apoptosis; these effects were reversed by\n                      <jats:italic>PTPRM<\/jats:italic>\n                      overexpression. In\u00a0vivo, exogenous\n                      <jats:italic>PTPRM<\/jats:italic>\n                      overexpression attenuated HPH progression in mice. Mechanistically,\n                      <jats:italic>PTPRM<\/jats:italic>\n                      directly targeted cell adhesion molecules (CAMs), which increased catenin production, thereby inhibiting abnormal cell proliferation and migration and promoting apoptosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our findings reveal a novel\n                      <jats:italic>lncRNA\u201092467<\/jats:italic>\n                      \/\n                      <jats:italic>miR\u2010205\u20105p<\/jats:italic>\n                      \/\n                      <jats:italic>PTPRM<\/jats:italic>\n                      \/\n                      <jats:italic>CAMs<\/jats:italic>\n                      regulatory axis in HPH pathogenesis. These results suggest that\n                      <jats:italic>PTPRM<\/jats:italic>\n                      may serve as a promising therapeutic target for HPH.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ame2.70267","type":"journal-article","created":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T04:18:58Z","timestamp":1786421938000},"page":"1913-1927","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genome\u2010wide network analysis identifies the\n                    <i>lncRNA\u201092467\/miR\u2010205\u20105p\/PTPRM\/CAMs<\/i>\n                    axis in a rat model of hypoxic pulmonary hypertension"],"prefix":"10.1002","volume":"9","author":[{"given":"Yan\u2010Ying","family":"Shen","sequence":"first","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi\u2010Bing","family":"Chen","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Li","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiang","family":"Xu","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ge","family":"Guo","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Han\u2010Lu","family":"Li","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong\u2010Ming","family":"Yao","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun\u2010Lei","family":"Liu","sequence":"additional","affiliation":[{"name":"Medical Innovation Research Department of PLA General Hospital  Beijing P.R. 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