Evidence map›Paper›PMID 28388574›Full record

ArticleOncotarget2017

Over-expression of growth differentiation factor 15 (GDF15) preventing cold ischemia reperfusion (I/R) injury in heart transplantation through Foxo3a signaling.

Yixin Zhang, Lisa A Moszczynski, Qing Liu, Jifu Jiang, Duo Zhao, Douglas Quan, Tina Mele, Vivian McAlister, Anthony Jevnikar, Seung Joon Baek and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. ATF5-Dependent GDF15 Expression Mediates Anesthesia-Induced Neuroprotection Against Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

12 authors at 5 institutions in 3 countries.

Yixin ZhangDepartment of Cardiovascular Surgery, The Second Hospital, Jilin University, Changchun, China.
Lisa A MoszczynskiDepartment of Pathology, Western University, Ontario, Canada.
Qing LiuDepartment of Cardiovascular Surgery, The Second Hospital, Jilin University, Changchun, China.
Jifu JiangDepartment of Pathology, Western University, Ontario, Canada.
Duo ZhaoDepartment of Cardiovascular Surgery, The Second Hospital, Jilin University, Changchun, China.
Douglas QuanDepartment of Surgery, Western University, Ontario, Canada.
Tina MeleDepartment of Surgery, Western University, Ontario, Canada.
Vivian McAlisterDepartment of Surgery, Western University, Ontario, Canada.
Anthony JevnikarLawson Health Research Institute, Ontario, Canada.
Seung Joon BaekDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA.
Kexiang LiuDepartment of Cardiovascular Surgery, The Second Hospital, Jilin University, Changchun, China.
Xiufen ZhengDepartment of Pathology, Western University, Ontario, Canada.
Western University · CASecond Affiliated Hospital of Jilin University · CNLawson Health Research Institute · CALondon Health Sciences Centre · CAUniversity of Tennessee at Knoxville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia reperfusion (I/R) injury which inevitably occurs during heart transplantation is the major factor leading to organ failure and graft rejection. In order to develop new therapies to prevent I/R injury, we used both a murine heart transplantation model with 24 hour cold I/R and an in vitro cell culture system to determine whether growth differentiation factor 15 (GDF15) is a protective factor in preventing I/R injury in heart transplantation and to further investigate underlying mechanisms of I/R injury. We found that cold I/R caused severe damage to the endocardium, epicardium and myocardium of heart grafts from wild type C57BL/6 mice, whereas grafts from GDF15 transgenic (TG) mice showed less damage as demonstrated by decreased cell apoptosis/death, decreased neutrophils infiltration and the preservation of the normal structure of the heart. Over-expression of GDF15 reduced expression of phosphorylated RelA p65, pre-inflammatory and pro-apoptotic genes while it enhanced Foxo3a phosphorylation in vitro and in vivo. Over-expression of GDF15 inhibited cell apoptosis/death and reduced neutrophil infiltration. In conclusion, this study, for the first time, demonstrates that GDF15 is a promising target for preventing cold I/R injury in heart transplantation. This study also shows that the resultant protective effects are mediated by the Foxo3 and NFκB signaling pathways.

Indexed as

Gene ExpressionHeart TransplantationAnimalsApoptosisCold IschemiaCytokinesForkhead Box Protein O3Growth Differentiation Factor 15HumansInflammation MediatorsMaleMiceMyocytes, CardiacPeroxidasePhosphorylationRatsCytokinesForkhead Box Protein O3Growth Differentiation Factor 15Inflammation MediatorsPeroxidaseFoxo3aGDF15heart transplantationischemia reperfusion injury

Identifiers

PMID28388574
PMCPMC5482674
OpenAlexW2600842773

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.