ArticleJHLT open2025
Gene expression analysis of primary graft dysfunction in adult heart transplant recipients: A cohort study.
Article in JHLT open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- From the Bench to the Bedside and Back: Contemporary Applications of Basic Science to Innovations in Heart Transplantation.The Canadian journal of cardiology · 2026Review
- Long-Term Outcome of Myocardial Protection in Heart Transplantation: Comparison Among 3 Different Solutions.Interdisciplinary cardiovascular and thoracic surgery · 2026Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cardiac transplantation remains the primary treatment for advanced heart failure, with primary graft dysfunction (PGD) being the leading cause of early mortality. While PGD's exact pathogenesis is unclear, ischemia/reperfusion injury is a key factor. Donor hearts undergo multiple stresses, such as brain death, hypothermia, and ischemia, contributing to PGD and reduced graft survival. Many centers are studying PGD's pathophysiology through epidemiological, biomarker, and transcriptome analyses. This study aims to evaluate, via transcriptomic analysis of myocardial biopsies, the gene expression profile of patients with PGD and compare it with those without PGD. Methods: Adult heart transplant patients were included in the study after signing the Informed Consent. The diagnosis of PGD followed the International Society for Heart and Lung Transplant criteria. Clinical and laboratory data from donors and recipients were evaluated. We included 20 consecutive heart transplant patients in the protocol. Gene expression analysis was performed via biopsies at donor heart implantation. Results: Eleven genes had their expression significantly different in patients with PGD, with MYL4 the less expressed gene, and related to the myosin function and the gene B3GALT 5 the most expressed one and associated with the inflammatory response. Conclusions: The gene expression in patients with PGD is different when compared to patients without PGD. MYL4 gene was much less expressed in these patients and B3GALT5 was overexpressed. Future studies regarding gene expression on PGD may clarify the pathophysiology and provide possible biomarkers of the disease.
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