ArticleESC heart failure2021
Human myocardial mitochondrial oxidative capacity is impaired in mild acute heart transplant rejection.
Article in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Ischaemia-Reperfusion Injury in Organ Transplantation: Role of Coenzyme Q10.Journal of clinical medicine · 2025Review
- METAB-HTX: prospective, longitudinal cohort study evaluating cardiac and systemic metabolism after heart transplantation.ESC heart failure · 2025Article
- Myocardial inflammation is associated with impaired mitochondrial oxidative capacity in ischaemic cardiomyopathy.ESC heart failure · 2025Article
- Elamipretide: A Review of Its Structure, Mechanism of Action, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Histopathological Characteristics of Percutaneous Endomyocardial Biopsy in Heart Transplant Rejection Surveillance: A Single Center Experience.Biomedicines · 2024Article
- Unveiling the invisible: Is there a role of CMR in biopsy-negative graft dysfunction post-heart transplantation?ESC heart failure · 2024Article
- Peripheral Blood Mononuclear Cells Mitochondrial Respiration and Superoxide Anion after Heart Transplantation.Journal of clinical medicine · 2022Article
- Human myocardial mitochondrial oxidative capacity is impaired in mild acute heart transplant rejection.ESC heart failure · 2021Article
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAcute cellular rejection (ACR) following heart transplantation (HTX) is associated with long-term graft loss and increased mortality. Disturbed mitochondrial bioenergetics have been identified as pathophysiological drivers in heart failure, but their role in ACR remains unclear. We aimed to prove functional disturbances of myocardial bioenergetics in human heart transplant recipients with mild ACR by assessing myocardial mitochondrial respiration using high-resolution respirometry, digital image analysis of myocardial inflammatory cell infiltration, and clinical assessment of HTX patients. We hypothesized that (i) mild ACR is associated with impaired myocardial mitochondrial respiration and (ii) myocardial inflammation, systemic oxidative stress, and myocardial oedema relate to impaired mitochondrial respiration and myocardial dysfunction. METHODS AND
resultsWe classified 35 HTX recipients undergoing endomyocardial biopsy according International Society for Heart and Lung Transplantation criteria to have no (0R) or mild (1R) ACR. Additionally, we quantified immune cell infiltration by immunohistochemistry and digital image analysis. We analysed mitochondrial substrate utilization in myocardial fibres by high-resolution respirometry and performed cardiovascular magnetic resonance (CMR). ACR (1R) was diagnosed in 12 patients (34%), while the remaining 23 patients revealed no signs of ACR (0R). Underlying cardiomyopathies (dilated cardiomyopathy 50% vs. 65%; P = 0.77), comorbidities (type 2 diabetes mellitus: 50% vs. 35%, P = 0.57; chronic kidney disease stage 5: 8% vs. 9%, P > 0.99; arterial hypertension: 59% vs. 30%, P = 0.35), medications (tacrolimus: 100% vs. 91%, P = 0.54; mycophenolate mofetil: 92% vs. 91%, P > 0.99; prednisolone: 92% vs. 96%, P > 0.99) and time post-transplantation (21.5 ± 26.0 months vs. 29.4 ± 26.4 months, P = 0.40) were similar between groups. Mitochondrial respiration was reduced by 40% in ACR (1R) compared with ACR (0R) (77.8 ± 23.0 vs. 128.0 ± 33.0; P < 0.0001). Quantitative assessment of myocardial CD3
conclusionsMild ACR with inflammatory cell infiltration associates with impaired mitochondrial bioenergetics in cardiomyocytes. Our findings may help to identify novel checkpoints in cardiac immune metabolism as potential therapeutic targets in post-transplant care.
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