ArticleBMC anesthesiology2025
Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via the LncRNA FAM201A/miR-488-3p/PTEN axis.
Article in BMC anesthesiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Protective Effect of Isoflurane on Hypoxia/Reoxygenation-Induced Myocardial Injury via miR-548a-5p Regulation of PTEN.Journal of biochemical and molecular toxicology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMyocardial ischemia-reperfusion injury (IRI) remains a major clinical challenge, and sevoflurane (Sevo) preconditioning has shown cardioprotective effects. However, the underlying molecular mechanisms are incompletely understood. This study aimed to determine whether Sevo alleviates hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury by regulating the lncRNA FAM201A.
methodsTo investigate the cardioprotective effects of Sevo, an optimized in vitro H/R model with Sevo preconditioning was established using H9c2 cardiomyocytes. FAM201A expression was modulated via overexpression plasmids, and miR-488-3p levels were altered using miRNA mimics in combination with Sevo exposure. Cell apoptosis, membrane integrity (cTnI, CK-MB), inflammatory responses (IL-6, TNF-α), and oxidative stress markers (SOD, MDA) were assessed. Bioinformatics prediction and dual-luciferase reporter assays validated interactions between FAM201A, miR-488-3p, and their target gene PTEN. Western blot analysis evaluated PI3K/AKT pathway activity.
resultsH/R significantly increased FAM201A expression in cardiomyocytes, which was dose-dependently suppressed by Sevo pretreatment. Overexpression of FAM201A abolished the protective effects of Sevo, as evidenced by exacerbated apoptosis rates, aggravated oxidative stress, and heightened inflammatory cytokine levels. Mechanistically, FAM201A directly interacted with and negatively regulated miR-488-3p. miR-488-3p mimics counteracted FAM201A-induced cellular damage and suppressed PTEN expression, a validated target of miR-488-3p. Furthermore, Sevo-mediated PTEN downregulation and subsequent AKT phosphorylation were reversed by FAM201A overexpression but rescued by miR-488-3p restoration.
conclusionsSevo preconditioning protects against H/R injury by downregulating FAM201A, which sponges miR-488-3p to reduce PTEN and activate PI3K/AKT signaling. Targeting this axis may provide potential therapeutic targets for IRI.
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.