ArticleJournal of molecular histology2025
Theaflavin-3,3'-digallate protects against myocardial ischemia/reperfusion injury and hypoxia/reoxygenation injury by activating the PI3K/Akt/mTOR pathway.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- Tea consumption and cardiovascular risk and outcomes: mechanistic insights, epidemiological evidence, and clinical implications.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia followed by reperfusion triggers a range of pathological events, among which excessive autophagy plays a key role. Theaflavin-3,3'-digallate (TF3) is a functional polyphenol of black tea and is beneficial in the prevention or/and treatment of various diseases. Here, we explored the therapeutic effect of TF3 on myocardial ischemia/reperfusion (I/R) injury. I/R injury was induced in rats through ischemia (30 min) followed by reperfusion (24 h). TF3 was administered seven days before the I/R. Cardiac function was determined by echocardiography. Infarct size and apoptosis were assessed using TTC and TUNEL, respectively. H9C2 cardiomyocytes were treated with TF3 or/and PI3K inhibitor (LY294002) and then exposed to hypoxia/reoxygenation (H/R). Content levels of myocardial injury indicators in rat hearts and H9C2 cardiomyocytes were detected using corresponding kits. H9C2 cardiomyocyte apoptosis was evaluated by flow cytometry. Protein levels of autophagy, apoptosis, and PI3K/Akt/mTOR signaling in vivo and in vitro were detected using western blotting. TF3 reduced myocardial infarct size and decreased serum CK-MB, cTnT, and LDH content levels in rat model of myocardial I/R. TF3 reduced apoptosis and autophagy in I/R rat hearts and H9C2 cardiomyocytes by reducing Bax, cleaved caspase-3, Beclin-1, and LC3B levels, and elevating Bcl-2 and p62 levels. TF3 administration activated PI3K/Akt/mTOR signaling in I/R rat hearts and H9C2 cells. PI3K inhibitor LY294002 reversed the inhibitory effect of TF3 on H/R-induced apoptosis and autophagy in H9C2 cells. Overall, TF3 alleviates I/R-induced myocardial injury by reducing autophagy and apoptosis by activating PI3K/Akt/mTOR signaling.
Indexed as
Identifiers
40576913What 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.