Evidence map›Paper›PMID 22673889›Full record

ArticleKidney international2012

Abrogation of lectin-like oxidized LDL receptor-1 attenuates acute myocardial ischemia-induced renal dysfunction by modulating systemic and local inflammation.

Jingjun Lu, Xianwei Wang, Wenze Wang, Harish Muniyappa, Abhishek Deshmukh, Changping Hu, Kumuda Das, Jawahar L Mehta

Open access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

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  11. Toward Human Models of Cardiorenal SyndromeFrontiers in cardiovascular medicine · 2022
    Review
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  20. Myocardial infarction causes inflammation and leukocyte recruitment at remote sites in the myocardium and in the renal glomerulus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013
    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

8 authors at 2 institutions in 2 countries.

Jingjun LuDepartment of Emergency Medicine, Renmin Hospital of Wuhan University, Wuhan, China. lvjingjun@gmail.com
Xianwei Wang
Wenze Wang
Harish Muniyappa
Abhishek Deshmukh
Changping Hu
Kumuda Das
Jawahar L Mehta
Central Arkansas Veterans Healthcare System · USWuhan University · CN

Funding

Endothelial dysfunction in aged Trx-deficient mice.R01HL107885 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI DAS, KUMUDA C · 2011 to 2014
$1.8M
Protective role of thioredoxin in endothelial apoptosis in the heart in ischemia-R01HL109397 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI DAS, KUMUDA C · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL107885NHLBI NIH HHS R01 HL109397
6 · The paper itself

Abstract

It is assumed that acute myocardial infarction affects renal function. To study the mechanism, we used mice following permanent ligation of their left coronary artery that results in extensive myocardial infarction. Soon after ligation, there was a marked rise in circulating pro-inflammatory cytokines and malondialdehyde (thiobarbituric acid-positive evidence of lipid peroxidation). Renal function had significantly declined by the third day in association with mild fibrosis, and swelling of glomeruli and tubules. There was a significant increase in the expression of the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), interelukin-1β, vascular cell adhesion molecule-1, and thiobarbituric acid-reactive substances in the kidney. Renal function showed some recovery by Day 21; however, there was progressive fibrosis of the kidneys. LOX-1 knockout mice had significantly diminished increases in systemic and renal pro-inflammatory cytokines, malondialdehyde, structural alterations, and decline in renal function than the wild-type mice following ligation of the left coronary artery. Cardiac function and survival rates were also significantly better in the LOX-1 knockout mice than in the wild-type mice. Hence, severe myocardial ischemia results in renal dysfunction and histological abnormalities suggestive of acute renal injury. Thus, LOX-1 is a key modulator among multiple mechanisms underlying renal dysfunction following extensive myocardial infarction.

Indexed as

AnimalsBlood PressureCollagenCytokinesDisease Models, AnimalFibrosisGlomerular Filtration RateInflammationInflammation MediatorsKidneyKidney DiseasesLipid PeroxidationMalondialdehydeMiceMice, Inbred C57BLMice, KnockoutCollagenCytokinesInflammation MediatorsMalondialdehydeOlr1 protein, mouseScavenger Receptors, Class E

Identifiers

PMID22673889
PMCPMC4045456
OpenAlexW1998536767

What OpenQuestion holds

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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.