Evidence map›Paper›PMID 23499374›Full record

ArticleThe American journal of pathology2013

Kruppel-like factor 2 is a transcriptional regulator of chronic and acute inflammation.

Lalitha Nayak, Lediana Goduni, Yoichi Takami, Nikunj Sharma, Parul Kapil, Mukesh K Jain, Ganapati H Mahabeleshwar

Registry-linked trialAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02824471 (Sickle Cell Disease), which is not on this map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
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.

NCT02824471 recruitingnot on this mapstarted 2014, after this paper: background citation

Sickle Cell Disease (SCD) Biochip': Towards a Simple and Reliable Way to Monitor Sickle Cell Disease

TypeobservationalSponsorUniversity Hospitals Cleveland Medical CenterRan2014 to 2028Enrolled100ConditionsSickle Cell DiseaseArmsSCD Group
3 · Its place in the literature

Who cites it

42 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Inflammation in glomerular diseases.Frontiers in immunology · 2025
    Review
  8. KLF feedback loops in innate immunity.Frontiers in immunology · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors.

Lalitha NayakCase Cardiovascular Research Institute, Department of Medicine, Harrington Heart and Vascular Institute, Cleveland, Ohio; Division of Hematology and Oncology, Case Western Reserve University School of Medicine, University Hospitals Case Medical Center, Cleveland, Ohio.
Lediana Goduni
Yoichi Takami
Nikunj Sharma
Parul Kapil
Mukesh K Jain
Ganapati H Mahabeleshwar

Funding

KLF2, monocyte activation and vascular inflammationR01HL086548 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2007 to 2016
$3.5M
KLF2 as a regulator of endothelial cell biologyR01HL076754 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2004 to 2012
$3.2M
KLF4, Monocyte Biology and Vasculary InjuryR01HL075427 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2004 to 2010
$2.6M
KLF15 as novel regulator of cardiomyocyte biologyR01HL084154 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2007 to 2010
$1.5M
KLF15, TGFb1 and smooth muscle cell biologyR01HL072952 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI JAIN, MUKESH KUMAR · 2004 to 2007
$1.5M
KLF2 Mediated HIF-1 Regulation and Macrophage ActivationR00HL097023 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI MAHABALESHWAR, GANAPATI HOLANAGADDE · 2011 to 2013
$735k
KLF2 Mediated HIF-1 Regulation and Macrophage ActivationK99HL097023 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI MAHABALESHWAR, GANAPATI HOLANAGADDE · 2009 to 2010
$180k
NHLBI NIH HHS HL084154NHLBI NIH HHS HL086548NHLBI NIH HHS HL097023NHLBI NIH HHS HL72952NHLBI NIH HHS HL75427NHLBI NIH HHS HL76754NHLBI NIH HHS K99 HL097023NHLBI NIH HHS R00 HL097023NHLBI NIH HHS R01 HL072952NHLBI NIH HHS R01 HL075427NHLBI NIH HHS R01 HL076754NHLBI NIH HHS R01 HL084154NHLBI NIH HHS R01 HL086548
6 · The paper itself

Abstract

Although myeloid cell activation is requisite for an optimal innate immune response, this process must be tightly controlled to prevent collateral host tissue damage. Kruppel-like factor 2 (KLF2) is a potent regulator of myeloid cell proinflammatory activation. As an approximately 30% to 50% reduction in KLF2 levels has been observed in human subjects with acute or chronic inflammatory disorders, we studied the biological response to inflammation in KLF2(+/-) mice. Herein, we show that partial deficiency of KLF2 modulates the in vivo response to acute (sepsis) and subacute (skin) inflammatory challenge. Mechanistically, we link the anti-inflammatory effects of KLF2 to the inhibition of NF-κB transcriptional activity. Collectively, the observations provide biologically relevant insights into KLF2-mediated modulation of these inflammatory processes that could potentially be manipulated for therapeutic gain.

Indexed as

Transcription, GeneticAcute DiseaseAnimalsCarrageenanCell LineChronic DiseaseDisease Models, AnimalDisease ProgressionEdemaGene Expression RegulationHemizygoteHumansInflammationKruppel-Like Transcription FactorsLipopolysaccharidesMiceCarrageenanKlf2 protein, mouseKruppel-Like Transcription FactorsLipopolysaccharidesNF-kappa B

Identifiers

PMID23499374
PMCPMC3644709

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.