Evidence map›Paper›PMID 32896815›Full record

ArticleThe Journal of surgical research2021

Modulation of Interleukin-1 and -18 Mediated Injury in Donation after Circulatory Death Mouse Hearts.

Mohammed Quader, Eleonora Mezzaroma, Kristine Kenning, Stefano Toldo

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

Article in The Journal of surgical research, 2021. 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
1.8field-weighted citation impact, top 14% 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, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Innate and adaptive immunity in acute myocarditis.International journal of cardiology · 2024
    Review
  5. Review
  6. NormothermicFrontiers in cardiovascular medicine · 2023
    Article
  7. Article
  8. Review
  9. NLRP3 Inflammasome Inhibitors in Cardiovascular Diseases.Molecules (Basel, Switzerland) · 2021
    Review
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

4 authors at 1 institution in 1 country.

Mohammed QuaderCardiovascular Surgery, Virginia Commonwealth University, Richmond, Virginia; Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia. Electronic address: mohammed.quader@vcuhealth.org.
Eleonora MezzaromaPauley Heart Center, Virginia Commonwealth University, Richmond, Virginia; School of Pharmacy, Virginia Commonwealth University, Richmond, Virginia.
Kristine KenningCardiovascular Surgery, Virginia Commonwealth University, Richmond, Virginia.
Stefano ToldoPauley Heart Center, Virginia Commonwealth University, Richmond, Virginia; Division of Cardiology, Virginia Commonwealth University, Richmond, Virginia.
Virginia Commonwealth University · US

Funding

Unconventional IL-1 Signaling in Heart failureR01HL150115 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ABBATE, ANTONIO, TOLDO, STEFANO · 2020 to 2024
$1.9M
Reduction of cardiac injury in DCD hearts with prolonged ischemic period: Role of MPTP opening and calpain activationI01BX003859 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI QUADER, MOHAMMED · 2018 to 2025
–
BLRD VA I01 BX003859NHLBI NIH HHS R01 HL150115
6 · The paper itself

Abstract

backgroundDonation after circulatory death donors (DCD) can expand the donor pool for heart transplantation, which primarily depends on brain death donors. Ischemia and reperfusion injury are inherent to the DCD process. We hypothesize that pharmacologic inhibition of interleukin-1 (IL-1) and/or IL-18 is protective to DCD hearts. MATERIALS AND

methodsFollowing clinical protocol, in-situ ischemia time in control beating-heart donor (CBD) and DCD groups was less than 5 and 40 min, respectively. Wild type (WT) C57Bl6/j, IL-1 receptor type I knockout (IL-1RI-KO), and IL-18 KO mice were used. Hearts were reanimated for 90 min on a Langendorff system with Krebs-Henseleit buffer at 37°C, to assess physiologic parameters. Recombinant IL-1 receptor antagonist (IL-1Ra) and/or IL-18 binding protein (IL-18BP) were added to the Krebs-Henseleit buffer to inhibit IL-1 and/or the IL-18 signaling, respectively.

resultsDeveloped pressure and ± dP/dt were significantly impaired in the DCD-WT group compared to CBD-WT (P ≤ 0.05). Troponin release was higher in DCD-WT groups. Functional parameters were preserved, and troponin release was significantly less in the DCD knockout groups. Heart function was improved in DCD groups treated with IL-1Ra or IL-18BP compared to the DCD-WT group.

conclusionsHeart function was significantly impaired in the DCD-WT group compared to CBD-WT. Genetic deletion or pharmacologic blockade of IL-1 or IL-18 was protective to DCD hearts.

Indexed as

Tissue and Organ ProcurementAnimalsDeathDrug Evaluation, PreclinicalHeartIntercellular Signaling Peptides and ProteinsInterleukin-18Interleukin-1betaInterleukin 1 Receptor Antagonist ProteinMaleMiceMice, KnockoutMyocardial Reperfusion InjuryRandom AllocationIL1B protein, mouseIntercellular Signaling Peptides and ProteinsInterleukin-18interleukin-18 binding proteinInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinDonation after circulatory deathHeart transplantationIL-1IL-18Ischemia and reperfusion

Identifiers

PMID32896815
PMCPMC8687874
OpenAlexW3083215899

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.