Evidence map›Paper›PMID 23799145›Full record

ArticlePloS one2013

Angiotensin II receptor blocker attenuates intrarenal renin-angiotensin-system and podocyte injury in rats with myocardial infarction.

Zhu-zhi Wen, Mu-yan Cai, Zun Mai, Dong-mei Jin, Yang-xin Chen, Hui Huang, Deng-feng Geng, Jing-feng Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Therapeutic potential ofFrontiers in pharmacology · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Circadian rhythm of blood pressure and the renin-angiotensin system in the kidney.Hypertension research : official journal of the Japanese Society of Hypertension · 2017
    Review
  11. Cellular senescence in renal ageing and disease.Nature reviews. Nephrology · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Corilagin Alleviates Ang II-Induced Cardiac Fibrosis by Regulating the PTEN/AKT/mTOR Pathway.Dose-response : a publication of International Hormesis Society
    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 1 country.

Zhu-zhi WenDepartment of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Mu-yan Cai
Zun Mai
Dong-mei Jin
Yang-xin Chen
Hui Huang
Deng-feng Geng
Jing-feng Wang
Sun Yat-sen University · CNSun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms and mediators underlying common renal impairment after myocardial infarction (MI) are still poorly understood. The present study aimed to test the hypothesis that angiotensin II type 1 receptor blockers (ARBs) provides renoprotective effects after MI by preventing augmented intrarenal renin-angiotensin-system (RAS)-induced podocyte injury. Sprague-Dawley rats that underwent ligation of their coronary arteries were treated with losartan (20 mg/kg/d) or vehicle for 3 or 9 weeks. Renal function, histology and molecular changes were assessed. The current study revealed that MI-induced glomerular podocyte injury was identified by increased immunostaining for desmin and p16(ink4a), decreased immunostaining for Wilms' tumor-1 and podocin mRNA expression, and an induced increase of blood cystatin C at both 3 and 9 weeks. These changes were associated with increased intrarenal angiotensin II levels and enhanced expressions of angiotensinogen mRNA and angiotensin II receptor mRNA and protein. These changes were also associated with decreased levels of insulin-like growth factor (IGF-1) and decreased expressions of IGF-1 receptor (IGF-1R) protein and mRNA and phosphorylated(p)-Akt protein at 9 weeks, as well as increased expressions of 8-hydroxy-2'-deoxyguanosine at both time points. Treatment with losartan significantly attenuated desmin- and p16(ink4a)-positive podocytes, restored podocin mRNA expression, and decreased blood cystatin C levels. Losartan also prevented RAS activation and oxidative stress and restored the IGF-1/IGF-1R/Akt pathway. In conclusion, ARBs prevent the progression of renal impairment after MI via podocyte protection, partially by inhibiting the activation of the local RAS with subsequent enhanced oxidative stress and an inhibited IGF-1/IGF-1R/Akt pathway.

Indexed as

Angiotensin Receptor AntagonistsAnimalsCellular SenescenceGene ExpressionInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsKidneyLosartanMaleMembrane ProteinsMyocardial InfarctionOxidative StressPodocytesRatsRats, Sprague-DawleyReceptor, IGF Type 1Angiotensin Receptor AntagonistsInsulin-Like Growth Factor IIntracellular Signaling Peptides and ProteinsLosartanMembrane ProteinsNPHS2 proteinReceptor, IGF Type 1

Identifiers

PMID23799145
PMCPMC3682995
OpenAlexW2029227068

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.