ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
NET-DNA Activates the ANXA2/TMEM215/BiP Axis to Promote Mitophagy-Mediated Anoikis Resistance in Endometriosis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- NET-DNA Activates the ANXA2/TMEM215/BiP Axis to Promote Mitophagy-Mediated Anoikis Resistance in Endometriosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Endometriosis (EMs) features ectopic implantation of endometrial stromal cells (EESCs) and strong anoikis resistance, yet how inflammatory signals reprogram mitochondrial function remains unclear. Here, neutrophil extracellular traps (NETs), particularly their DNA scaffold (NET-DNA), are identified as enriched in early lesions and associated with enhanced mitophagy and EESCs survival. In primary human EESCs, NET-DNA suppresses anoikis, increases mitochondrial membrane potential, decreases reactive oxygen species, and enhances ER-mitochondria contacts. NET-DNA directly binds Annexin A2 (ANXA2), promotes its redistribution from the plasma membrane to the cytoplasm, and independently upregulates the ER-resident transmembrane protein TMEM215. TMEM215 facilitates formation of a Ca2+-dependent ANXA2-TMEM215 complex, enhancing ER-mitochondria contacts and PINK1/Parkin-mediated mitophagy. Silencing ANXA2 or TMEM215 disrupts mitophagy, impairs mitochondrial Ca2+ handling, reduces ER-mitochondria contacts, and restores anoikis sensitivity. Proteomic analysis identifies Binding Immunoglobulin Protein (BiP/GRP78) as a TMEM215-interacting partner, and NET-DNA promotes assembly of a TMEM215-ANXA2-BiP complex that reinforces mitochondrial quality control. In mouse EMs models, knockdown of TMEM215 or ANXA2 reduces lesion growth and partially reverses LPS-associated progression. These findings reveal a mechanism linking inflammation to mitochondrial reprogramming in EMs and suggest a potential therapeutic target.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.