ArticleExperimental & molecular medicine2026
Bone marrow stromal cells promote chemoresistance in acute myeloid leukaemia through P2RX7-mediated antioxidant defence.
Article in Experimental & molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukaemia (AML) remains a therapeutically challenging malignancy owing to its high relapse rates and chemoresistance, often linked to elevated antioxidant defences. Here, we demonstrate that bone marrow stromal cells (BMSCs) confer chemoresistance in AML by upregulating the purinergic receptor P2RX7. Blocking P2RX7 restored chemosensitivity of AML cells. Mechanistically, BMSC-mediated P2RX7 overexpression induces calcium influx and mitochondrial calcium overload, triggering mitochondrial stress and a compensatory antioxidant response. This process involves mitochondrial phosphoglycerate mutase 5 (PGAM5) transducing reactive oxygen species signals, interfering with Keap1-Nrf2 complex formation and leading to Nrf2 stabilization, thereby enhancing cellular antioxidant defences. These findings identify a vital role of P2RX7 in the BMSC-driven redox adaptation programme that underlies AML chemoresistance and highlight P2RX7 signalling as a potential therapeutic target.
Indexed as
Identifiers
42693241What OpenQuestion 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 OpenQuestion graph.