ArticleThe Journal of thoracic and cardiovascular surgery2015
Oxidant stress regulatory genetic variation in recipients and donors contributes to risk of primary graft dysfunction after lung transplantation.
Article in The Journal of thoracic and cardiovascular surgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 35 citations in OpenAlex.
- NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024Review
- Recipient, donor, and surgical factors leading to primary graft dysfunction after lung transplant.Journal of thoracic disease · 2023Article
- Lung Transplantation, Pulmonary Endothelial Inflammation, and Ex-Situ Lung Perfusion: A Review.Cells · 2021Review
- Incidence of primary graft dysfunction is higher according to the new ISHLT 2016 guidelines and correlates with clinical and molecular risk factors.Journal of thoracic disease · 2021Article
- Early Graft Dysfunction after Lung Transplantation.Current pulmonology reports · 2018Article
- Genome-wide association study identifies loci and candidate genes for non-idiopathic pulmonary hypertension in Eastern Chinese Han population.BMC pulmonary medicine · 2018Article
- Recent advances in lung transplantation.F1000Research · 2018Review
- The Perioperative Lung Transplant Virome: Torque Teno Viruses Are Elevated in Donor Lungs and Show Divergent Dynamics in Primary Graft Dysfunction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017Article
- Primary graft dysfunction: pathophysiology to guide new preventive therapies.Expert review of respiratory medicine · 2017Review
- Effects of Glutathione S-Transferase Gene Polymorphisms and Antioxidant Capacity per Unit Albumin on the Pathogenesis of Chronic Obstructive Pulmonary Disease.Oxidative medicine and cellular longevity · 2017Article
- DNA methylation profiling in peripheral lung tissues of smokers and patients with COPD.Clinical epigenetics · 2017Article
- An Endothelial Hsp70-TLR4 Axis Limits Nox3 Expression and Protects Against Oxidant Injury in Lungs.Antioxidants & redox signaling · 2016Article
- Mechanisms of lung ischemia-reperfusion injury.Current opinion in organ transplantation · 2016Review
- Common variants of NFE2L2 gene predisposes to acute respiratory distress syndrome in patients with severe sepsis.Critical care (London, England) · 2015Article
- One step closer to the elimination of primary graft dysfunction.The Journal of thoracic and cardiovascular surgery · 2015Article
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveOxidant stress pathway activation during ischemia reperfusion injury may contribute to the development of primary graft dysfunction (PGD) after lung transplantation. We hypothesized that oxidant stress gene variation in recipients and donors is associated with PGD.
methodsDonors and recipients from the Lung Transplant Outcomes Group (LTOG) cohort were genotyped using the Illumina IBC chip filtered for oxidant stress pathway genes. Single nucleotide polymorphisms (SNPs) grouped into SNP sets based on haplotype blocks within 49 oxidant stress genes selected from gene ontology pathways and literature review were tested for PGD association using a sequencing kernel association test. Analyses were adjusted for clinical confounding variables and population stratification.
resultsThree hundred ninety-two donors and 1038 recipients met genetic quality control standards. Thirty percent of patients developed grade 3 PGD within 72 hours. Donor NADPH oxidase 3 (NOX3) was associated with PGD (P = .01) with 5 individual significant loci (P values between .006 and .03). In recipients, variation in glutathione peroxidase (GPX1) and NRF-2 (NFE2L2) was significantly associated with PGD (P = .01 for both). The GPX1 association included 3 individual loci (P values between .006 and .049) and the NFE2L2 association included 2 loci (P = .03 and .05). Significant epistatic effects influencing PGD susceptibility were evident between 3 different donor blocks of NOX3 and recipient NFE2L2 (P = .026, P = .017, and P = .031).
conclusionsOur study has prioritized GPX1, NOX3, and NFE2L2 genes for future research in PGD pathogenesis, and highlights a donor-recipient interaction of NOX3 and NFE2L2 that increases the risk of PGD.
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