{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T09:28:25Z","timestamp":1792747705933,"version":"4.5.0"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2021,4,20]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Antenatal intrauterine fetal hypoxia is a common pregnancy complication that has profound adverse effects on an individual's vascular health later in life. Pulmonary arteries are sensitive to hypoxia, but adverse effects of antenatal hypoxia on pulmonary vasoreactivities in the offspring remain unknown. This study aimed to determine the effects and related mechanisms of antenatal hypoxia on pulmonary artery functions in adult male offspring.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Pregnant Sprague\u2010Dawley rats were housed in a normoxic or hypoxic (10.5% O\n              <jats:sub>2<\/jats:sub>\n              ) chamber from gestation days 10 to 20. Male offspring were euthanized at 16\u00a0weeks old (adult offspring). Pulmonary arteries were collected for vascular function, electrophysiology, target gene expression, and promoter methylation studies. In pulmonary artery rings, contractions to serotonin hydrochloride, angiotensin II, or phenylephrine were reduced in the antenatal hypoxic offspring, which resulted from inactivated L\u2010type Ca\n              <jats:sup>2+<\/jats:sup>\n              channels. In pulmonary artery smooth muscle cells, the basal whole\u2010cell Ca\n              <jats:sup>2+<\/jats:sup>\n              currents, as well as vasoconstrictor\u2010induced Ca\n              <jats:sup>2+<\/jats:sup>\n              transients were significantly reduced in antenatal hypoxic offspring. In addition, increased promoter methylations within L\u2010type Ca\n              <jats:sup>2+<\/jats:sup>\n              channel subunit alpha1 C were compatible with its reduced expressions.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              This study indicated that antenatal hypoxia programmed long\u2010lasting vascular hypocontractility in the male offspring that is linked to decreases of L\u2010type Ca\n              <jats:sup>2+<\/jats:sup>\n              channel subunit alpha1 C in the pulmonary arteries. Antenatal hypoxia resulted in pulmonary artery adverse outcomes in postnatal offspring, was strongly associated with reprogrammed L\u2010type Ca\n              <jats:sup>2+<\/jats:sup>\n              channel subunit alpha1 C expression via a DNA methylation\u2010mediated epigenetic mechanism, advancing understanding toward the effect of antenatal hypoxia in early life on long\u2010term vascular health.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.120.019922","type":"journal-article","created":{"date-parts":[[2021,4,10]],"date-time":"2021-04-10T09:33:20Z","timestamp":1618047200000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":13,"title":["Antenatal Hypoxia Affects Pulmonary Artery Contractile Functions via Downregulating L\u2010type Ca\n            <sup>2+<\/sup>\n            Channels Subunit Alpha1 C in Adult Male Offspring"],"prefix":"10.1161","volume":"10","author":[{"given":"Huan","family":"Li","sequence":"first","affiliation":[{"name":"From the Institute for Fetology First Hospital of Soochow University Suzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bingyu","family":"Ji","sequence":"additional","affiliation":[{"name":"From the Institute for Fetology First Hospital of Soochow University Suzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ting","family":"Xu","sequence":"additional","affiliation":[{"name":"From the Institute for Fetology First Hospital of Soochow University Suzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meng","family":"Zhao","sequence":"additional","affiliation":[{"name":"From the Institute for Fetology First Hospital of Soochow University Suzhou 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