<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Qin L</submitter><funding>MOST | National Natural Science Foundation of China (NSFC)</funding><funding>Special Fund for Scientific and Technological Innovation Talent Teams of Shanxi Province</funding><funding>MOST | National Natural Science Foundation of China</funding><pagination>e2409597121</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11536148</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>121(44)</volume><pubmed_abstract>Epidemiological studies show a strong correlation between air pollution and fetal growth restriction (FGR), but existing results are controversial due to inherent limitations, such as causality of specific pollutants, developmental origin, and maternal-fetal transmission. To address this controversy, we first conducted a retrospective analysis of 28,796 newborns and revealed that maternal nitrogen dioxide (NO&lt;sub>2&lt;/sub>) exposure during the second trimester was positively associated with FGR, with an adjusted odds ratio of 1.075 (95% confidence interval: 1.020-1.133) per 10 μg/m&lt;sup>3&lt;/sup> NO&lt;sub>2&lt;/sub> increase for small for gestational age. Then, by establishing an animal model of prenatal NO&lt;sub>2&lt;/sub> exposure, we confirmed its adverse effects on embryonic growth and hematopoiesis </pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Maternal NO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; exposure and fetal growth restriction: Hypoxia transmission and lncRNAs-proinflammation-mediated abnormal hematopoiesis.</pubmed_title><pmcid>PMC11536148</pmcid><funding_grant_id>No.22206164</funding_grant_id><funding_grant_id>No.22276117</funding_grant_id><funding_grant_id>No.22036005</funding_grant_id><funding_grant_id>No. 202204051002024</funding_grant_id><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Qin L</pubmed_authors><pubmed_authors>Ma L</pubmed_authors><pubmed_authors>Guo Y</pubmed_authors><pubmed_authors>Li D</pubmed_authors><pubmed_authors>He J</pubmed_authors><pubmed_authors>Sang N</pubmed_authors><pubmed_authors>YiXi Z</pubmed_authors><pubmed_authors>Gong Z</pubmed_authors><pubmed_authors>Yue H</pubmed_authors><pubmed_authors>Yan W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Maternal NO&amp;lt;sub&amp;gt;2&amp;lt;/sub&amp;gt; exposure and fetal growth restriction: Hypoxia transmission and lncRNAs-proinflammation-mediated abnormal hematopoiesis.</name><description>Epidemiological studies show a strong correlation between air pollution and fetal growth restriction (FGR), but existing results are controversial due to inherent limitations, such as causality of specific pollutants, developmental origin, and maternal-fetal transmission. To address this controversy, we first conducted a retrospective analysis of 28,796 newborns and revealed that maternal nitrogen dioxide (NO&lt;sub>2&lt;/sub>) exposure during the second trimester was positively associated with FGR, with an adjusted odds ratio of 1.075 (95% confidence interval: 1.020-1.133) per 10 μg/m&lt;sup>3&lt;/sup> NO&lt;sub>2&lt;/sub> increase for small for gestational age. Then, by establishing an animal model of prenatal NO&lt;sub>2&lt;/sub> exposure, we confirmed its adverse effects on embryonic growth and hematopoiesis </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-06-01T05:19:11.855Z</modification><creation>2026-04-08T09:25:33.971Z</creation></dates><accession>S-EPMC11536148</accession><cross_references><pubmed>39432779</pubmed><doi>10.1073/pnas.2409597121</doi></cross_references></HashMap>