ArticleFrontiers in endocrinology2022
Grim-19 deficiency promotes decidual macrophage autophagy in recurrent spontaneous abortion.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Autophagy in PE: Dispute, Role and Potential Target.Cell proliferation · 2025Review
- Impact of endocrine disrupting chemicals on macrophages at the maternal-fetal interface.Seminars in immunopathology · 2025Review
- Immune dysregulation of decidual NK cells mediated by GRIM19 downregulation contributes to the occurrence of recurrent pregnancy loss.Molecular and cellular biochemistry · 2025Article
- Obesity and recurrent spontaneous abortion: the crucial role of weight management in pregnancy.Reproductive biology and endocrinology : RB&E · 2025Review
- Angelica sinensis polysaccharide as potential protectants against recurrent spontaneous abortion: focus on autophagy regulation.Frontiers in medicine · 2025Article
- Stage-specific autophagy dynamics in reproductive processes and associated disorders.Frontiers in cell and developmental biology · 2025Review
- Feasibility study on the use of "Qi-tonifying medicine compound" as an anti-fatigue functional food ingredient based on network pharmacology and molecular docking.Frontiers in nutrition · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
Dysregulation of decidual macrophages leads to the occurrence of recurrent spontaneous abortion (RSA). However, the role of macrophages in RSA occurrence remains unclear. In this study, we found that the expression of Grim-19 was decreased, and the expression of autophagy related proteins Beclin1, LC3B II/I and BNIP3 was markedly upregulated in decidual macrophages of RSA patients compared with the normal pregnancy group. Furthermore, we demonstrated that downregulation of GRIM-19 increased the expression of autophagy related proteins Beclin1, LC3B II/I, BNIP3 and the proinflammatory cytokines IL1B, IL6 and TNFa in uterine mononuclear cells of
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