ArticleJournal of cellular and molecular medicine2022
TNFα-induced abnormal activation of TNFR/NF-κB/FTH1 in endometrium is involved in the pathogenesis of early spontaneous abortion.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Super-enhancer-driven KIAA1522 upregulation suppresses ferroptosis in hepatocellular carcinoma.Clinical and translational medicine · 2026Article
- Multi-Omics Analysis Reveals Inflammatory Activation and Maternal-Fetal Interface Remodeling in Spontaneous Abortion.Current medical science · 2026Article
- MicroRNA-155 targets p65 to regulate PD-L1 expression in the early pregnancy endometrium.Scientific reports · 2025Article
- Association of maternal thyroid peroxidase antibody during pregnancy with placental morphology and inflammatory and oxidative stress responses.Frontiers in endocrinology · 2023Article
- TNFα-induced abnormal activation of TNFR/NF-κB/FTH1 in endometrium is involved in the pathogenesis of early spontaneous abortion.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Early spontaneous abortion (ESA) is one of the most common complications during pregnancy and the inflammation condition in uterine environment such as long-term exposure to high TNFα plays an essential role in the aetiology. Ferritin heavy chain (FTH1) is considered to be closely associated with inflammation and very important in normal pregnancy, yet the underlying mechanism of how TNFα induced abortion and its relationship with FTH1 remain elusive. In this study, we found that TNFα and FTH1 were positively expressed in decidual stromal cells and increased significantly in the ESA group compared with the normal pregnancy group (NP group). Besides, TNFα expression was positively correlated with FTH1 expression. Furthermore, in vitro cell model demonstrated that high TNFα could induce the abnormal signals of TNFR/NF-κB/FTH1 and activate apoptosis both in human endometrium stromal cells (hESCs) and in local decidual tissues. Taken together, the present findings suggest that the excessive apoptosis in response to TNFα-induced upregulation of FTH1 may be responsible for the occurrence of ESA, and thus provide a possible therapeutic target for the treatment of ESA.
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