ArticleJournal of cellular and molecular medicine2026
Thymoquinone Protects Against Cardiac Hypertrophy via PPAR-γ/PI3K/Akt Pathway.
Article in Journal of cellular and molecular medicine, 2026. 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.
- Thymoquinone Protects Against Cardiac Hypertrophy via PPAR-γ/PI3K/Akt Pathway.Journal of cellular and molecular medicine · 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
11 authors.
Funding
Abstract
Thymoquinone (TQ), the principal active constituent of Nigella stativa, has demonstrated numerous biological properties and therapeutic effects on various diseases. However, its therapeutic potential against cardiac hypertrophy remains uncertain. This study aims to investigate the protective effects of TQ on stress-induced cardiac hypertrophy and elucidate the underlying mechanisms. Our findings reveal that TQ mitigates stress-induced cardiac hypertrophy in mice and AngII-induced hypertrophy in H9c2 cells. Moreover, TQ inhibits cardiomyocyte ferroptosis and apoptosis by downregulating PTGS2, Bax, and upregulating GPX4, Bcl-2, thereby alleviating cardiac hypertrophy and dysfunction. Mechanistically, the protective effects of TQ against ferroptosis and apoptosis in cardiac hypertrophy were reversed by the PPAR-γ inhibitor (GW9662). In addition, TQ treatment led to increased protein expression levels of P-PI3K and P-AKt. Taken together, our findings suggest that TQ could attenuate cardiac hypertrophy through activation of the PPAR-γ/PI3K/Akt signalling 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.