ArticleMolecular biology reports2026
APEX1 attenuates myocardial ischemia-reperfusion injury by inhibiting ferroptosis via the Nrf2/GPX4 signaling pathway.
Article in Molecular biology reports, 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
8 authors.
Funding
Abstract
backgroundMyocardial ischemia reperfusion injury (MIRI) is a primary cause of poor prognosis in patients with myocardial infarction, with ferroptosis being a significant form of cell death in this process. Apurinic/apyrimidinic endonuclease 1 (APEX1) is a multifunctional protein involved in DNA repair and redox activation of transcription factors and has shown therapeutic potential in ischemic heart disease. This study aims to investigate whether APEX1 protects against MIRI by inhibiting ferroptosis and to explore the underlying mechanisms.
methodsA rat model of myocardial ischemia/reperfusion (I/R) and a H9c2 cell model of hypoxia/reoxygenation (H/R) were established. APEX1 protein levels were assessed in both models. The protective effects of APEX1 against ferroptosis were evaluated by measuring ferroptosis-associated proteins, Fe²⁺ levels, and lipid peroxidation markers. To explore the mechanistic pathway, the Nrf2 inhibitor ML385 was employed to examine whether the protective effects of APEX1 were mediated through the Nrf2/GPX4 signaling axis.
resultsAPEX1 protein levels were significantly reduced in both the rat I/R model and the H9c2 cell H/R model. APEX1 mitigated MIRI-induced ferroptosis through exogenous pathways, including inhibition of iron transporters TfR1 and FTH1, and endogenous pathways, such as GPX4 activity. Inhibition of Nrf2 using ML385 partially reversed the protective effects of APEX1 against ferroptosis and reduced GPX4 expression, indicating the involvement of the Nrf2/GPX4 signaling pathway.
conclusionThis study demonstrates that APEX1 protects against MIRI by inhibiting ferroptosis through activation of the Nrf2/GPX4 signaling pathway. These findings identify APEX1 as a promising therapeutic target for the treatment of MIRI.
Indexed as
Identifiers
42470514What 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.