ArticleSmall (Weinheim an der Bergstrasse, Germany)2026
Multifunctional Manganese-Based Nanocomposites for Enhanced Immunotherapy by Regulating Lactate Metabolism and Activating the cGAS-STING Pathway.
Article in Small (Weinheim an der Bergstrasse, Germany), 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
4 authors.
Funding
Abstract
The efficacy of tumor immunotherapy is frequently hindered by immunosuppressive tumor microenvironments (TME). Activating the cyclic guanosine monophosphate-adenosine monophosphate synthase stimulator of interferon genes (cGAS-STING) pathway and depleting the tumor metabolic byproduct lactate offer promising strategies to reverse the immunosuppressive TME and enhance immunotherapy efficacy. In this study, multifunctional honeycomb manganese oxide nanocomposites (AL@hM) loaded with banoxantrone (AQ4N) and lactate oxidase are designed to activate the cGAS-STING pathway and deplete lactate for achieving potent cancer immunotherapy. Upon internalization by tumor cells, lactate oxidase catalyzes the oxidation of lactate, generating hydrogen peroxide and exacerbating hypoxia, thereby reducing lactate levels within both tumor cells and the TME. This lactate depletion promotes cGAS activation and immunosuppressive TME reprogramming. Concurrently, hypoxia-mediated toxic 1,4-diazabicyclo[2.2.2]octane-1,4-dione (AQ4) production and manganese ions-driven reactive oxygen species generation facilitate the accumulation of cytosolic double-stranded DNA (dsDNA). These processes collectively enhance the sensitivity of manganese ions-dsDNA-cGAS recognition, leading to robust activation of the cGAS-STING pathway and strong immune response. This study presents an innovative strategy that combines activation of the cGAS-STING pathway and lactate metabolism regulation to remodel the tumor immune microenvironment for potentiating immunotherapy outcomes.
Indexed as
Identifiers
What 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.