Evidence map›Paper›PMID 30761731›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2019

Circulating mitochondria in organ donors promote allograft rejection.

Liwen Lin, He Xu, Muath Bishawi, FeiFei Feng, Kannan Samy, George Truskey, Andrew S Barbas, Allan D Kirk, Todd V Brennan

Open access · hybridAbstract 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, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 9% 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

58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

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  10. Mitochondrial Transplantation as a Therapeutic Strategy for Inherited Mitochondrial Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Liwen LinDepartments of Surgery, Duke University Medical Center, Durham, North Carolina.
He XuDepartments of Surgery, Duke University Medical Center, Durham, North Carolina.
Muath BishawiDepartments of Surgery, Duke University Medical Center, Durham, North Carolina.ORCID 0000-0002-8906-3600
FeiFei FengDepartment of Toxicology, Zhengzhou University, Zhengzhou, China.
Kannan SamyDepartments of Surgery, Duke University Medical Center, Durham, North Carolina.
George TruskeyBiomedical Engineering, Duke University Medical Center, Durham, North Carolina.ORCID 0000-0002-6885-4489
Andrew S BarbasDepartments of Surgery, Duke University Medical Center, Durham, North Carolina.ORCID 0000-0003-3476-2313
Allan D KirkDepartments of Surgery, Duke University Medical Center, Durham, North Carolina.ORCID 0000-0003-2004-5962
Todd V BrennanDepartment of Surgery, Cedars-Sinai Medical Center, Los Angeles, California.ORCID 0000-0002-0480-2989
Duke Medical Center · USCedars-Sinai Medical Center · USZhengzhou University · CN

Funding

Stimulating Access to Research in Residency (StARR) - NHLBIR38HL143612 · NHLBI · DUKE UNIVERSITY · PI Mai ElMallah, David H. Harpole · 2018 to 2026
$2.6M
T Cell Maturation and the Nexus of Viral- and Allo-ImmunityR01AI097423 · NIAID · EMORY UNIVERSITY · PI KIRK, ALLAN D. · 2012 to 2016
$2.6M
Role of Endogenous Toll-Like Receptor Ligands in Allospecific T Cell ActivationK08AI101263 · NIAID · DUKE UNIVERSITY · PI BRENNAN, TODD VICTOR · 2012 to 2016
$644k
NHLBI NIH HHS R38 HL143612NIAID NIH HHS K08 AI101263NIAID NIH HHS L30 AI090991NIAID NIH HHS R01 AI097423
6 · The paper itself

Abstract

The innate immune system is a critical regulator of the adaptive immune responses that lead to allograft rejection. It is increasingly recognized that endogenous molecules released from tissue injury and cell death are potent activators of innate immunity. Mitochondria, ancestrally related to bacteria, possess an array of endogenous innate immune-activating molecules. We have recently demonstrated that extracellular mitochondria are abundant in the circulation of deceased organ donors and that their presence correlates with early allograft dysfunction. Here we demonstrate the ability of mitochondria to activate endothelial cells (ECs), the initial barrier between a solid organ allograft and its host. We find that mitochondria exposure leads to the upregulation of EC adhesion molecules and their production of inflammatory cytokines and chemokines. Additionally, mitochondrial exposure causes dendritic cells to upregulate costimulatory molecules. Infusion of isolated mitochondria into heart donors leads to significant increase in allograft rejection in a murine heterotopic heart transplantation model. Finally, co-incubation of human peripheral blood mononuclear cells with mitochondria-treated ECs results in increased numbers of effector (IFN-γ

Indexed as

AllograftsGraft RejectionMitochondria, HeartTissue DonorsAnimalsCell AdhesionCells, CulturedHeart TransplantationHumansMiceMice, Inbred BALB CMice, Inbred C57BLT-Lymphocytesadhesion molecules/integrinsbasic (laboratory) research/sciencedonors and donationheart transplantation/cardiologyimmunobiologyimmunosuppression/immune modulationtranslational research/science

Identifiers

PMID30761731
PMCPMC6591073
OpenAlexW2914675066

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.