Evidence map›Paper›PMID 28743964›Full record

ArticleScientific reports2017

Toll-like Receptor 4 Deficiency Reduces Oxidative Stress and Macrophage Mediated Inflammation in Hypertensive Kidney.

Sathnur Pushpakumar, Lu Ren, Sourav Kundu, Alejandra Gamon, Suresh C Tyagi, Utpal Sen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 82 citations in OpenAlex.

  1. Sex differences in TLR4 expression in SHR do not contribute to sex differences in blood pressure or the renal T cell profile.American journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Oxidative Stress and Age-Related Tumors.Antioxidants (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Article
  9. A new immune disease: systemic hypertension.Clinical kidney journal · 2023
    Review
  10. Review
  11. Review
  12. Review
  13. Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

6 authors at 3 institutions in 2 countries.

Sathnur PushpakumarDepartment of Physiology, University of Louisville School of Medicine, Louisville, KY-40202, USA.
Lu RenDepartment of Physiology, University of Louisville School of Medicine, Louisville, KY-40202, USA.
Sourav KunduInstitute of Advanced Study in Science and Technology, Guwahati, Assam, 781035, India.
Alejandra GamonUniversity of California, San Diego, CA, 92093, USA.
Suresh C TyagiDepartment of Physiology, University of Louisville School of Medicine, Louisville, KY-40202, USA.
Utpal SenDepartment of Physiology, University of Louisville School of Medicine, Louisville, KY-40202, USA. utpal.sen@louisville.edu.
University of Louisville · USInstitute of Advanced Study in Science and Technology · INUniversity of California, San Diego · US

Funding

Hydrogen sulfide mechanism of renal hypertensionR01DK104653 · NIDDK · UNIVERSITY OF LOUISVILLE · PI SEN, UTPAL, TYAGI, SURESH C. · 2015 to 2018
$2.5M
Homocysteine & Angiotensin II in Renovascular RemodelingR01HL104103 · NHLBI · UNIVERSITY OF LOUISVILLE · PI SEN, UTPAL · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL104103NIDDK NIH HHS R01 DK104653
6 · The paper itself

Abstract

Oxidative stress and inflammation are integral to hypertension-induced renal injury. A unifying feature for the two components is Toll-like receptors (TLR), which are key regulators of the innate immune system. Recent studies implicate TLR4 activation and oxidative stress in cardiovascular diseases and also as a link between inflammation and hypertension. However, its role in hypertension induced renal injury remains unexplored. In the present study, we investigated whether TLR-4 deficiency reduces Ang-II-induced renal injury and fibrosis by attenuating reactive oxygen species (ROS) production and inflammation. C3H/HeOuJ mice with normal TLR-4 and C3H/HeJ

Indexed as

Angiotensin IIAnimalsCytokinesDisease Models, AnimalHypertensionMacrophagesMiceMice, Inbred C3HOxidative StressRenal Insufficiency, ChronicSignal TransductionToll-Like Receptor 4Transforming Growth Factor betaVascular ResistanceAngiotensin IICytokinesTlr4 protein, mouseToll-Like Receptor 4Transforming Growth Factor beta

Identifiers

PMID28743964
PMCPMC5526876
OpenAlexW2736908489

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.