ArticleInternational journal of biological sciences2025
ANXA6 Overexpression Causes Abnormal Decidual Macrophage-Trophoblast Crosstalk in Recurrent Spontaneous Abortion.
Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- ALKBH5 Positively Regulates BMP2 to Influence Endometrial Decidualization in Recurrent Spontaneous Abortion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Direct and indirect evidence for pyroptosis and immune dysregulation in IVF/ICSI-ET-related early pregnancy loss.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
ANXA6 is involved in numerous biological processes; however, its association with recurrent spontaneous abortion (RSA) remains poorly understood. In this study, we observed significant upregulation of ANXA6 expression in decidual macrophages from RSA patients. Functional analysis revealed that ANXA6 overexpression enhanced reactive oxygen species (ROS) generation and reduced mitochondrial membrane potential, thereby promoting pyroptosis and upregulating M1 macrophage polarization markers. Mechanistically, inhibition of NLRP3 rescued ANXA6 overexpression-induced elevation of M1 polarization and pyroptosis in macrophages. In addition, inhibition of ROS alleviated the decreased mitochondrial membrane potential, aggravated macrophage pyroptosis, and exacerbated inflammatory response, as well as the promoted macrophage M1 polarization caused by ANXA6 overexpression. Further mechanisms suggest that overexpression of ANXA6 in macrophages could promote the accumulation of mitochondrial ROS and inhibit mitochondrial membrane potential through the NF-κB signaling pathway, exacerbating macrophage pyroptosis and amplifying the resulting inflammatory response, thereby promoting macrophage M1 polarization. Besides, ANXA6 overexpressing macrophages showed an inhibitory effect on trophoblast function
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