Evidence map›Paper›PMID 19370315›Full record

ArticleMolecular and cellular biochemistry2009

Valsartan preconditioning protects against myocardial ischemia-reperfusion injury through TLR4/NF-kappaB signaling pathway.

Jian Yang, Hong Jiang, Jun Yang, Jia-Wang Ding, Li-Hua Chen, Song Li, Xiao-Dong Zhang

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

44 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
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  6. Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023
    Review
  7. Effects of Lycopene Attenuating Injuries in Ischemia and Reperfusion.Oxidative medicine and cellular longevity · 2022
    Review
  8. MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Heart Failure in Type 2 Diabetes Mellitus.Circulation research · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Effect of Hexadecyl Azelaoyl Phosphatidylcholine on Cardiomyocyte Apoptosis in Myocardial Ischemia-Reperfusion Injury: A Hypothesis.Medical science monitor : international medical journal of experimental and clinical research · 2018
    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

7 authors at 3 institutions in 1 country.

Jian YangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Hong Jiang
Jun Yang
Jia-Wang Ding
Li-Hua Chen
Song Li
Xiao-Dong Zhang
Renmin Hospital of Wuhan University · CNChina Three Gorges University · CNYichang Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor 4 (TLR4) activation has been implicated in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. The activated TLR4 is capable of activating a variety of proinflammatory mediators, such as tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6). Valsartan as a kind of Angiotensin II type 1 receptor blockers is gradually used for the treatment of ischemic heart disease depending on its anti-inflammation function. Therefore, we hypothesized that valsartan protects against myocardial I/R injury by suppressing TLR4 activation. We constructed the rat model of myocardial I/R injury. The rats were pretreated with valsartan for 2 weeks, and then subjected to 30 min ischemia and 2 h reperfusion. TLR4 and Nuclear factor kappa-B (NF-kappaB) levels were detected by quantitative real-time PCR and western blot. In order to evaluate myocardial damage, the myocardial infarct size, histopathologic changes, and the release of myocardial enzymes, proinflammation cytokines and Angiotensin II were analyzed by triphenyl tetrazolium chloride (TTC) staining, light microscopy, and enzyme-linked immunosorbent assay (ELISA), respectively. Valsartan preconditioning inhibited TLR4 and NF-kappaB expressions concomitant with an improvement in myocardial injury, such as smaller infarct size, fewer release of myocardial enzymes, and proinflammation mediators. These findings suggest that valsartan plays a pivotal role in the protective effects on myocardial I/R injury. This protection mechanism is possibly due to its anti-inflammation function via TLR4/NF-kappaB signaling pathway.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsInflammation MediatorsIschemic Preconditioning, MyocardialMyocardial Reperfusion InjuryNF-kappa BRatsSignal TransductionTetrazolesToll-Like Receptor 4Treatment OutcomeValineValsartanAngiotensin II Type 1 Receptor BlockersInflammation MediatorsNF-kappa BTetrazolesTLR4 protein, humanToll-Like Receptor 4ValineValsartan

Identifiers

PMID19370315
OpenAlexW1966944979

What OpenQuestion holds

Textmetadata
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.