ReviewInternational journal of molecular sciences2025
Primary Graft Dysfunction in Lung Transplantation: An Overview of the Molecular Mechanisms.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Trem1 regulates neutrophil metabolism and recruitment in lung ischemia-reperfusion injury.Redox biology · 2026Article
- Anti-heparanase shields against endothelial dysfunction in a rat model of warm pulmonary ischemia-reperfusion.Respiratory research · 2026Article
- 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary graft dysfunction (PGD) remains a major complication after lung transplantation. Donor lung ischemia followed by reperfusion drives oxidative stress and inflammatory responses. The pathophysiology is influenced by various donor-, procedure-, and recipient-related factors, which complicates the identification of biomarkers for evaluation of donor lung injury or therapeutic interventions to minimize PGD. This review provides an overview of the molecular pathways that contribute to PGD pathophysiology, including those involved in loss of endothelial-epithelial membrane integrity, neutrophil infiltration, and the development of pulmonary edema.
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Registered trials
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