ArticleMolecular medicine reports2025
Metformin alleviates lung ischemia‑reperfusion injury via the SIRT1 pathway following lung transplantation in diabetic rats.
Article in Molecular medicine reports, 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.
- Lung Ischemia-Reperfusion Injury in Lung Transplant Surgery: Where Do We Stand?Antioxidants (Basel, Switzerland) · 2025Review
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
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus (DM) exacerbates lung ischemia‑reperfusion (IR) injury and leads to poor survival in lung transplantation recipients. Metformin protects a number of tissues from IR injury. The present study aimed to investigate the effect of metformin on diabetic lung IR injury and the potential mechanisms. Rats with type 2 DM were exposed to metformin with or without administration of EX527, an inhibitor of the silent information regulator 1 (SIRT1) pathway, following lung transplantation. Lung function, alveolar‑capillary permeability, inflammatory response, oxidative stress, cell apoptosis, mitochondrial function, mitochondrial biogenesis key proteins and the SIRT1 signaling pathway were assessed. The effect of metformin on diabetic lung IR injury was evaluated by ELISA, oxidative stress assays, immunofluorescence, flow cytometry, TUNEL assay and western blotting. The results demonstrated that DM was associated with a significant increase in the IR‑induced alveolar‑capillary permeability, inflammatory response, oxidative stress and cell apoptosis. Furthermore, DM was associated with a significant decrease in mitochondrial function and biogenesis, SIRT1 expression and lung function. Metformin treatment markedly attenuated diabetic lung IR injury by alleviating the inflammatory response, oxidative stress and cell apoptosis, preserving mitochondrial function, and promoting mitochondrial biogenesis. However, EX527 inhibited the protective effect of metformin. In conclusion, metformin alleviated the inflammatory response, oxidative stress and cell apoptosis, preserved mitochondrial function, and promoted mitochondrial biogenesis via the activation of the SIRT1 pathway in diabetic lung IR injury.
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.