Evidence map›Paper›PMID 27659428›Full record

ArticleScientific reports2016

Prevention of allograft rejection in heart transplantation through concurrent gene silencing of TLR and Kinase signaling pathways.

Hongmei Wang, Xusheng Zhang, Xiufen Zheng, Zhu Lan, Jun Shi, Jifu Jiang, Terry Zwiep, Qing Li, Douglas Quan, Zhu-Xu Zhang and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
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  7. Article
  8. Is There a Positive Side to T Cell Exhaustion?Frontiers in immunology · 2019
    Review
  9. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Hongmei WangInstitute of Immunotherapy and Medical College of Nanchang University, and Jiangxi Academy of Medical Sciences, Nanchang, China.
Xusheng ZhangDepartment of Surgery, Pathology, and Oncology, University of Western Ontario, London, Canada.
Xiufen ZhengDepartment of Surgery, Pathology, and Oncology, University of Western Ontario, London, Canada.
Zhu LanMulti-Organ Transplant Program, London Health Sciences Centre, London, Canada.
Jun ShiInstitute of Immunotherapy and Medical College of Nanchang University, and Jiangxi Academy of Medical Sciences, Nanchang, China.
Jifu JiangMulti-Organ Transplant Program, London Health Sciences Centre, London, Canada.
Terry ZwiepDepartment of Surgery, Pathology, and Oncology, University of Western Ontario, London, Canada.
Qing LiInstitute of Immunotherapy and Medical College of Nanchang University, and Jiangxi Academy of Medical Sciences, Nanchang, China.
Douglas QuanDepartment of Surgery, Pathology, and Oncology, University of Western Ontario, London, Canada.
Zhu-Xu ZhangInstitute of Immunotherapy and Medical College of Nanchang University, and Jiangxi Academy of Medical Sciences, Nanchang, China.
Weiping MinInstitute of Immunotherapy and Medical College of Nanchang University, and Jiangxi Academy of Medical Sciences, Nanchang, China.
London Health Sciences Centre · CAWestern University · CAJiangxi Provincial Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) act as initiators and conductors responsible for both innate and adaptive immune responses in organ transplantation. The mammalian target of rapamycin (mTOR) is one of the most critical signaling kinases that affects broad aspects of cellular functions including metabolism, growth, and survival. Recipients (BALB/c) were treated with MyD88, TRIF and mTOR siRNA vectors, 3 and 7 days prior to heart transplantation and 7, 14 and 21 days after transplantation. After siRNA treatment, recipients received a fully MHC-mismatched C57BL/6 heart. Treatment with mTOR siRNA significantly prolonged allograft survival in heart transplantation. Moreover, the combination of mTOR siRNA with MyD88 and TRIF siRNA further extended the allograft survival; Flow cytometric analysis showed an upregulation of FoxP3 expression in spleen lymphocytes and a concurrent downregulation of CD40, CD86 expression, upregulation of PD-L1 expression in splenic dendritic cells in MyD88, TRIF and mTOR treated mice. There is significantly upregulated T cell exhaustion in T cells isolated from tolerant recipients. This study is the first demonstration of preventing immune rejection of allogeneic heart grafts through concurrent gene silencing of TLR and kinase signaling pathways, highlighting the therapeutic potential of siRNA in clinical transplantation.

Identifiers

PMID27659428
PMCPMC5034230
OpenAlexW2521151298

What OpenQuestion holds

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LicenceCC BY
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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.