ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2026
Electroacupuncture Alleviates Oxidative Stress and Cuproptosis in Metabolic Dysfunction-Associated Steatotic Liver Disease Mice Through Activation of the NRF2/ARE Pathway.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Oxidative stress and the newly characterized mode of regulated cell death, cuproptosis, drive the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Electroacupuncture (EA) is a promising non-drug treatment, but its mechanisms are unclear. This study investigated the benefits of EA in a high-fat diet (HFD)-induced MASLD mouse model, focusing on the NRF2/ARE pathway, cuproptosis, and the gut-liver axis. Methods: MASLD was established in C57BL/6J mice via a 16-week HFD. Mice were arbitrarily categorized into four groups: control (C, normal chow diet), model (M, HFD), EA (HFD + EA), and EA plus NRF2 inhibitor (EM, HFD + EA + inhibitor). A 4-week intervention was then conducted. Post-intervention, body weight alterations were tracked, and serum, liver tissue, and fecal specimens were gathered for subsequent examination. Results: EA treatment significantly improved the metabolic profile, reducing body weight, lipids, and hepatic inflammation. It attenuated oxidative stress by enhancing antioxidant capacity and activated the NRF2/ARE pathway. EA also modulated cuproptosis-related genes (upregulating dihydrolipoamide S-acetyltransferase (Dlat), downregulating solute carrier family 31 member 1 (Slc31a1), ferredoxin reductase (Fdx1), and heat shock protein 70 (Hsp70)). Furthermore, EA remodeled the gut microbiota (increasing Limosilactobacillusand Ligilactobacillus) and elevated related metabolites. Conclusion: EA ameliorates MASLD through multiple mechanisms, including regulating lipid metabolism, attenuating inflammation and oxidative stress, activating NRF2, suppressing cuproptosis, and altering the gut-liver axis, collectively contributing to hepatic improvement.
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.