ArticleTransplantation direct2020
Rejection-associated Mitochondrial Impairment After Heart Transplantation.
Article in Transplantation direct, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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Who cites it
10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 9 citations in OpenAlex.
- Exploring mitochondrial health and transplantation strategies in DCD heart transplantation: a systematic review.Journal of translational medicine · 2025Pooled it
- Mitochondrial Consequences of Organ Preservation Techniques during Liver Transplantation.International journal of molecular sciences · 2021Pooled it
- Cellular and Molecular Changes Induced by Various Preservation Temperatures and Methods of Preservation in Renal Grafts and Other Solid Organ Grafts.International journal of molecular sciences · 2026Review
- Mitochondrial transplantation for delirium superimposed on dementia: from pathogenic mechanisms to clinical translation challenges.Frontiers in aging neuroscience · 2026Review
- Ischaemia-Reperfusion Injury in Organ Transplantation: Role of Coenzyme Q10.Journal of clinical medicine · 2025Review
- Out of the ice age: Preservation of cardiac allografts with a reusable 10 °C cooler.JTCVS open · 2024Article
- Unsupervised mRNA-seq classification of heart transplant endomyocardial biopsies.Clinical transplantation · 2023Article
- Microvesicular Steatosis and Severe Cardiac Allograft Dysfunction.Transplantation direct · 2022Article
- Human myocardial mitochondrial oxidative capacity is impaired in mild acute heart transplant rejection.ESC heart failure · 2021Article
- Transcriptomics in transplantation: More than just biomarkers of allograft rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial dysfunction is associated with poor allograft prognosis. Mitochondrial-related gene expression (GE) in endomyocardial biopsies (EMBs) could be useful as a nonimmune functional marker of rejection. We hypothesize that acute cardiac allograft rejection is associated with decreased mitochondrial-related GE in EMBs.
methodsWe collected 64 routines or clinically indicated EMB from 47 patients after heart transplant. The EMBs were subjected to mRNA sequencing. We conducted weighted gene coexpression network analysis to construct module-derived eigengenes. The modules were assessed by gene ontology enrichment and hub gene analysis. Modules were correlated with the EMBs following the International Society of Heart and Lung Transplantation histology-based criteria and a classification based on GE alone; we also correlated with clinical parameters.
resultsThe modules enriched with mitochondria-related and immune-response genes showed the strongest correlation to the clinical traits. Compared with the no-rejection samples, rejection samples had a decreased activity of mitochondrial-related genes and an increased activity of immune-response genes. Biologic processes and hub genes in the mitochondria-related modules were primarily involved with energy generation, substrate metabolism, and regulation of oxidative stress. Compared with International Society of Heart and Lung Transplantation criteria, GE-based classification had stronger correlation to the weighted gene coexpression network analysis-derived functional modules. The brain natriuretic peptide level, ImmuKnow, and Allomap scores had negative relationships with the expression of mitochondria-related modules and positive relationships with immune-response modules.
conclusionsDuring acute cardiac allograft rejection, there was a decreased activity of mitochondrial-related genes, related to an increased activity of immune-response genes, and depressed allograft function manifested by brain natriuretic peptide elevation. This suggests a rejection-associated mitochondrial impairment.
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Registered trials
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