ArticleScientific reports2026
LncRNA DLX6-AS1 promotes necroptosis through PI3K/AKT/mTOR signaling pathway in myocardial ischemia/reperfusion injury mice.
Article in Scientific 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/reperfusion injury (MIRI) leads to life-threatening myocardial infarction. Necroptosis is involved in MIRI. The lncRNA DLX6-AS1 was found to participate in the context of MIRI. In this article, we examined the effect of DLX6-AS1 on ischemia perfusion-induced myocardial injury caused by necroptosis and the underlying potential mechanism. We constructed a mouse model of MIRI, and hematoxylin-eosin staining, TUNEL staining, echocardiology, Western blotting (WB), and reverse transcriptase-polymerase chain reaction (RT‒PCR) were employed to evaluate myocardial infarction and necroptosis. Rat H9c2 cells were induced by hypoxia-reoxygenation (H/R), and we analyzed the possible mechanism by overexpressing and inhibiting DLX6-AS1 expression. Cell Counting Kit 8, lactate dehydrogenase (LDH), flow cytometry, RT‒PCR, and WB were utilized to examine cell injury, apoptosis, and relative protein expression. MIRI induced myocardial damage and impaired cardiac function in mice. Ischemia/reperfusion injury results in necroptosis, a process that Nec-1 inhibits. The mRNA levels of RIP1, RIP3, and MLKL were increased, and DLX6-AS1 demonstrated an increase in the IR model, indicating that DLX6-AS1 was associated with necroptosis. Furthermore, H/R-induced H9C2 cells exhibited high LDH levels, low cell activity, and severe apoptosis levels. DLX6-AS1 overexpression caused cell damage and necroptosis and increased the expression of proteins, including PI3K, p-PI3K, AKT, p-AKT, mTOR and p-mTOR. DLX6-AS1 inhibition suppressed necroptosis and cell damage through the PI3K/AKT/mTOR signaling pathway. Myocardial ischemia‒reperfusion injury induces necroptosis, and DLX6-AS1 promotes this process through the PI3K/AKT/mTOR signaling pathway.
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.