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Recent studies have highlighted the critical role of autophagy in the development of PE. However, the precise mechanisms underlying the upregulation of autophagy in PE remain unclear. This study demonstrated that the expression of the tumor suppressor p53\u2010binding protein 2 (TP53BP2) is significantly upregulated in patients with PE. Silencing of\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    not only decreases autophagy but also attenuates PE progression in rat model. Moreover,\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    expression was positively correlated with blood pressure and body mass index (BMI) but negatively correlated with gestational age at delivery and neonatal birth weight. Our findings suggest that\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    enhances autophagy by promoting the release of Beclin\u20101 from the Bcl\u20102\/Beclin\u20101 complex. Additionally, DNMT1 and G9a cooperatively downregulated\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    expression by reducing DNA methylation and H3K9me2 enrichment in the\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    promoter region. Importantly, the cooperation between DNMT1 and G9a suppressed E2F1 binding to the\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    promoter, leading to transcriptional repression of\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    in trophoblasts. In brief, our study indicates that\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    promotes autophagy in trophoblasts through DNA methylation and H3K9me2\u2010mediated transcriptional regulation. These findings suggest that targeting\n                    <jats:italic>TP53BP2<\/jats:italic>\n                    may be a potential therapeutic strategy for PE.\n                  <\/jats:p>","DOI":"10.1002\/advs.202516408","type":"journal-article","created":{"date-parts":[[2026,1,7]],"date-time":"2026-01-07T14:30:13Z","timestamp":1767796213000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["<i>TP53BP2<\/i>\n                    Promotes Placental Autophagy and Preeclampsia via G9a and\n                    <i>DNMT1<\/i>\n                    Cooperatively Modulating E2F1"],"prefix":"10.1002","volume":"13","author":[{"given":"Nan","family":"Jiang","sequence":"first","affiliation":[{"name":"School of Basic Medical Science Central South University  Changsha China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaoju","family":"Jin","sequence":"additional","affiliation":[{"name":"LuoHe Medical 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