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Background: Epstein-Barr virus (EBV) is a herpesvirus linked to nine different human tumors and lymphoproliferative disorders. Immunosuppression promotes EBV-driven malignancies. The most frequent EBV-induced malignancies are lymphomas and nasopharyngeal carcinoma. By promoting smooth muscle proliferation, EBV can induce EBV-associated smooth muscle tumors (EBV-SMT). EBV-SMT is a rare oncological entity for which no current guideline for diagnosis or management exists. Data on posttransplant EBV-SMT (PT-SMT) are scarce in kidney transplant recipients.
Methods: We conducted a national multicentric retrospective study and collected cases among transplantation centers in France. Kidney transplant recipients experiencing histologically proven PT-SMT were included. We collected data on demographic characteristics of patient, history of kidney transplantation, history of PT-SMT, evolution of graft function, and patient survival.
Results: Eight patients were included. The median age at PT-SMT diagnosis was 31 years (range 6.5-40). PT-SMT occurred after a median delay of 37.8 months after transplantation (range 6-175). PT-SMT management consisted in immunosuppressive regimen minimization in all patients. Introduction of mTOR inhibitors was performed in two patients. Four patients (50%) needed chemotherapy. Surgical resection was performed in four patients. At last follow-up after PT-SMT diagnosis (median 33 months (range 17-132)), five patients were considered in complete remission, and two patients had died. Two patients experienced graft rejection; two resumed dialysis (25%). All patients with available data presented with impaired graft function at last follow-up.
Conclusion: PT-SMT is a subacute and progressive disease during kidney transplantation. Even if the risk of developing PT-SMT is low in kidney transplant recipients (0.07% in our cohort), PT-SMT is associated with significant graft loss, possibly due to reduced immunosuppression. Developing guidelines could help transplantation teams better manage these patients.
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http://dx.doi.org/10.1111/ctr.15424 | DOI Listing |
J Interferon Cytokine Res
September 2025
Department of Nephrology, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Guangxi, China.
Hirudin, a polypeptide extracted from medicinal leeches, has demonstrated potential in treating renal fibrosis. This study aimed to explore the underlying mechanisms by which Hirudin alleviates renal fibrosis. Renal fibrosis models were established using unilateral ureteral obstruction (UUO) surgery in rats and transforming growth factor-β (TGF-β)-induced HK-2 cells, followed by treatment with different concentrations of Hirudin.
View Article and Find Full Text PDFCurr Drug Metab
September 2025
First School of Clinical Medicine, Yunnan University of Chinese Medicine, Kunming 650500, China.
Background: Tetrandrine (TET) demonstrates therapeutic potential for hypoxic pulmonary hypertension (HPH); however, its precise pharmacological mechanisms remain unclear. In this study, we aimed to investigate the effects of TET on pulmonary vascular remodeling (PVR) in HPH and elucidate the molecular pathways through which TET ameliorates HPH.
Methods: We established a rat model of HPH and evaluated the therapeutic effects of TET by measuring hemodynamic parameters, assessing right ventricular hypertrophy, and analyzing pathological changes in lung tissue.
Biomed Pharmacother
September 2025
Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Liver fibrosis, which eventually leads to cirrhosis, is characterized by excessive accumulation of type I collagen (COL1A), mainly derived from activated hepatic stellate cells (HSCs). Currently, there is no clinical treatments that can directly address this condition. The objectives of this study were to identify a compound that can suppress HSC activation and elucidate the molecular mechanism underlying its action.
View Article and Find Full Text PDFLung
September 2025
The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, 97 Lisburn Road, Belfast, Belfast BT9 7BL, UK.
Introduction: Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.
View Article and Find Full Text PDFImmunol Invest
September 2025
Respiratory and Critical Care Medicine, The 940th Hospital of Joint Logistics Support Force of chinese PLA, Lanzhou, China.
Background: Pulmonary neuroendocrine cells (PNECs) are specialized airway epithelial cells with dual sensory and secretory functions. They release bioactive mediators --including neuropeptides such as calcitonin gene-related peptide (CGRP) and gastrin-releasing peptide (GRP), and neurotransmitters such as 5-hydroxytryptamine (5-HT) and γ-aminobutyric acid (GABA) --that regulate airway smooth-muscle tone, mucus production, and immune responses. In chronic obstructive pulmonary disease (COPD), these PNEC-derived mediators contribute to airway inflammation, remodeling, and smooth-muscle dysfunction.
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