Evidence map›Paper›PMID 35583104›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2022

Extracellular vesicles derived from patients with antibody-mediated rejection induce tubular senescence and endothelial to mesenchymal transition in renal cells.

Rossana Franzin, Alessandra Stasi, Fabio Sallustio, Stefania Bruno, Guido Merlotti, Marco Quaglia, Giuseppe Grandaliano, Paola Pontrelli, Joshua M Thurman, Giovanni Camussi and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 36 citations in OpenAlex.

  1. High-flux hemodialysis with polymethylmethacrylate membranes reduces soluble CD40L, a mediator of cardiovascular disease in uremia.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 2 countries.

Rossana FranzinNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari Aldo Moro, Bari, Italy.ORCID 0000-0001-7907-7614
Alessandra StasiNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari Aldo Moro, Bari, Italy.ORCID 0000-0003-3652-3623
Fabio SallustioInterdisciplinary Department of Medicine (DIM), University of Bari "Aldo Moro", Bari, Italy.ORCID 0000-0002-5132-6532
Stefania BrunoDepartment of Medical Sciences and Molecular Biotechnology Center, University of Torino, Torino, Italy.ORCID 0000-0002-8879-9536
Guido MerlottiNephrology and Kidney Transplantation Unit, Department of Translational Medicine and Center for Autoimmune and Allergic Diseases (CAAD), University of Piemonte Orientale (UPO), Novara, Italy.ORCID 0000-0001-9069-6192
Marco QuagliaNephrology and Kidney Transplantation Unit, Department of Translational Medicine and Center for Autoimmune and Allergic Diseases (CAAD), University of Piemonte Orientale (UPO), Novara, Italy.ORCID 0000-0001-9423-9255
Giuseppe GrandalianoDepartment Translational Medicine and Surgery, Università Cattolica Sacro Cuore, Rome, Italy.ORCID 0000-0003-1213-2177
Paola PontrelliNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari Aldo Moro, Bari, Italy.ORCID 0000-0002-7654-8318
Joshua M ThurmanDepartment of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA.ORCID 0000-0002-3476-9956
Giovanni CamussiDepartment of Medical Sciences and Molecular Biotechnology Center, University of Torino, Torino, Italy.ORCID 0000-0003-2795-232X
Giovanni StalloneNephrology, Dialysis and Transplantation Unit, Advanced Research Center on Kidney Aging (A.R.K.A.), Department of Medical and Surgical Sciences, University of Foggia, Foggia, Italy.ORCID 0000-0002-2862-9017
Vincenzo CantaluppiNephrology and Kidney Transplantation Unit, Department of Translational Medicine and Center for Autoimmune and Allergic Diseases (CAAD), University of Piemonte Orientale (UPO), Novara, Italy.ORCID 0000-0002-4120-3555
Loreto GesualdoNephrology, Dialysis and Transplantation Unit, Department of Emergency and Organ Transplantation, University of Bari Aldo Moro, Bari, Italy.ORCID 0000-0002-4861-0911
Giuseppe CastellanoUnit of Nephrology, Dialysis and Renal Transplantation - Fondazione IRCCS Ca'Granda Ospedale Maggiore Policlinico di Milano, Milan, Italy.ORCID 0000-0002-0153-3795
University of Bari Aldo Moro · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Turin · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITUniversità Cattolica del Sacro Cuore · ITUniversity of Colorado Denver · USUniversity of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular vesicles (EV) are emerging mediators in several diseases. However, their role in the pathophysiology of antibody-mediated allograft rejection (AMR) has been poorly investigated. Here, we investigated the role of EV isolated from AMR patients in inducing tubular senescence and endothelial to mesenchymal transition (EndMT) and analyzed their miRNA expression profile. By multiplex bead flow cytometry, we characterized the immunophenotype of plasma AMR-derived EV and found a prevalent platelet and endothelial cell origin. In vitro, AMR-derived EV induced tubular senescence by upregulating SA-β Gal and CDKN1A mRNA. Furthermore, AMR-derived EV induced EndMT. The occurrence of tubular senescence and EndMT was confirmed by analysis of renal biopsies from the same AMR patients. Moreover, AMR-derived EV induced C3 gene upregulation and CFH downregulation in tubular epithelial cells, with C4d deposition on endothelial cells. Interestingly, RNase-mediated digestion of EV cargo completely abrogated tubular senescence and EndMT. By microarray analysis, miR-604, miR-515-3p, miR-let-7d-5p, and miR-590-3p were significantly upregulated in EV from AMR group compared with transplant controls, whereas miR-24-3p and miR-29a-3p were downregulated. Therefore, EV-associated miRNA could act as active player in AMR pathogenesis, unraveling potential mechanisms of accelerated graft senescence, complement activation and early fibrosis that might lead to new therapeutic intervention.

Indexed as

Extracellular VesiclesMicroRNAsEndothelial CellsEpithelial CellsHumansRNA, MessengerMicroRNAsMIRN515 microRNA, humanMIRN590 microRNA, humanRNA, Messengeragingantibody-mediated allograft rejectioncellular senescencecomplement systemextracellular vesiclesmiRNA

Identifiers

PMID35583104
PMCPMC9546277
OpenAlexW4280512011

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.