{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T09:36:50Z","timestamp":1790415410658,"version":"4.1.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2013,10,1]],"date-time":"2013-10-01T00:00:00Z","timestamp":1380585600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Human pulmonary artery smooth muscle cells (HPASMCs) express both adenosine monophosphate\u2013activated protein kinase (AMPK) \u03b11 and \u03b12. We investigated the distinct roles of AMPK \u03b11 and \u03b12 in the survival of HPASMCs during hypoxia and hypoxia-induced pulmonary hypertension (PH). The exposure of HPASMCs to hypoxia (3% O2) increased AMPK activation and phosphorylation, and the inhibition of AMPK with Compound C during hypoxia decreased their viability and increased lactate dehydrogenase activity and apoptosis. Although the suppression of either AMPK \u03b11 or \u03b12 expression led to increased cell death, the suppression of AMPK \u03b12 alone increased caspase-3 activity and apoptosis in HPASMCs exposed to hypoxia. It also resulted in the decreased expression of myeloid cell leukemia sequence 1 (MCL-1). The knockdown of MCL-1 or MCL-1 inhibitors increased caspase-3 activity and apoptosis in HPASMCs exposed to hypoxia. On the other hand, the suppression of AMPK \u03b11 expression alone prevented hypoxia-mediated autophagy. The inhibition of autophagy induced cell death in HPASMCs. Our results suggest that AMPK \u03b11 and AMPK \u03b12 play differential roles in the survival of HPASMCs during hypoxia. The activation of AMPK \u03b12 maintains the expression of MCL-1 and prevents apoptosis, whereas the activation of AMPK \u03b11 stimulates autophagy, promoting HPASMC survival. Moreover, treatment with Compound C, which inhibits both isoforms of AMPK, prevented and partly reversed hypoxia-induced PH in mice. Taking these results together, our study suggests that AMPK plays a key role in the pathogenesis of pulmonary arterial hypertension, and AMPK may represent a novel therapeutic target for the treatment of pulmonary arterial hypertension.<\/jats:p>","DOI":"10.1165\/rcmb.2012-0446oc","type":"journal-article","created":{"date-parts":[[2013,5,13]],"date-time":"2013-05-13T18:36:16Z","timestamp":1368470176000},"page":"609-618","source":"Crossref","is-referenced-by-count":68,"title":["Adenosine Monophosphate\u2013Activated Protein Kinase Is Required for Pulmonary Artery Smooth Muscle Cell Survival and the Development of Hypoxic Pulmonary Hypertension"],"prefix":"10.1093","volume":"49","author":[{"given":"Joyce Christina F.","family":"Ibe","sequence":"first","affiliation":[{"name":"Department of Pediatrics"},{"name":"Children\u2019s Hospital, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiyuan","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianji","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiyang","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Illinois at Chicago, University of Illinois Hospital and Health Sciences System, Chicago, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason X.-J.","family":"Yuan","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Illinois at Chicago, University of Illinois Hospital and Health Sciences System, Chicago, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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