Evidence map›Paper›PMID 27070323›Full record

ArticlePloS one2016

Modulation of Macrophage Polarization and HMGB1-TLR2/TLR4 Cascade Plays a Crucial Role for Cardiac Remodeling in Senescence-Accelerated Prone Mice.

Vengadeshprabhu Karuppagounder, Vijayasree V Giridharan, Somasundaram Arumugam, Remya Sreedhar, Suresh S Palaniyandi, Prasanna Krishnamurthy, Joao Quevedo, Kenichi Watanabe, Tetsuya Konishi, Rajarajan A Thandavarayan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

47 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Involvement of the SIRT1-NLRP3 pathway in the inflammatory response.Cell communication and signaling : CCS · 2023
    Review
  20. Extracellular Vesicles and Cardiac Aging.Advances in experimental medicine and biology · 2023
    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

10 authors at 5 institutions in 3 countries.

Vengadeshprabhu KaruppagounderDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
Vijayasree V GiridharanDepartment of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, TX 77054, United States of America.
Somasundaram ArumugamDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
Remya SreedharDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
Suresh S PalaniyandiDivision of Hypertension and Vascular Research, Henry Ford Health System, Detroit, MI 48202, United States of America.
Prasanna KrishnamurthyDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX 77030, United States of America.
Joao QuevedoDepartment of Psychiatry and Behavioral Sciences, The University of Texas Health Science Center at Houston, TX 77054, United States of America.
Kenichi WatanabeDepartment of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, Niigata 956-8603, Japan.
Tetsuya KonishiBasic studies on second generation functional foods, NUPALS Liaison R/D promotion division, Higashijima 265-1, Akiha-ku, Niigata, Japan.
Rajarajan A ThandavarayanDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX 77030, United States of America.
Niigata University of Pharmacy and Applied Life Sciences · JPHouston Methodist · USThe University of Texas Health Science Center at Houston · USChangchun University of Chinese Medicine · CNHenry Ford Health System · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
microRNA mediation of Endothelial Progenitor Cell function in Myocardial IchemiaR01HL116729 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KRISHNAMURTHY, PRASANNA · 2013 to 2017
$1.9M
NHLBI NIH HHS 1R01HL116729NHLBI NIH HHS R01 HL116729NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

The aim of this study was to investigate the role of macrophage polarization in aging heart. Macrophage differentiation is pathogenically linked to many inflammatory and immune disorders. It is often preceded by myocardial inflammation, which is characterized by increased cardiac damage and pro-inflammatory cytokine levels. Therefore, we investigated the hypothesis that senescence accelerated-prone (SAMP8) mice cardiac tissue would develop macrophage polarization compared with senescence-resistant control (SAMR1) mice. Both SAMP8 and SAMR1 mice were sacrificed when they became six month old. We evaluated, histo-pathological changes and modifications in protein expression by Western blotting and immuno-histochemical staining for M1 and M2 macrophage markers, high mobility group protein (HMG)B1 and its cascade proteins, pro-inflammatory factors and inflammatory cytokines in cardiac tissue. We observed significant upregulation of HMGB1, toll-like receptor (TLR)2, TLR4, nuclear factor (NF)κB p65, tumor necrosis factor (TNF)α, cyclooxygenase (COX)2, interferon (IFN)γ, interleukin (IL)-1β, IL-6 and M1 like macrophage specific marker cluster of differentiation (CD)68 expressions in SAMP8 heart. In contrast, M2 macrophage specific marker CD36, and IL-10 expressions were down-regulated in SAMP8 mice. The results from the study demonstrated that, HMGB1-TLR2/TLR4 signaling cascade and induction of phenotypic switching to M1 macrophage polarization in SAMP8 mice heart would be one of the possible reasons behind the cardiac dysfunction and thus it could become an important therapeutic target to improve the age related cardiac dysfunction.

Indexed as

AgingAnimalsCyclooxygenase 2HeartHMGB1 ProteinInflammationInterleukin-10Interleukin-1betaInterleukin-6MacrophagesMaleMiceNF-kappa BSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4Cyclooxygenase 2HMGB1 ProteinHMGB1 protein, mouseInterleukin-10Interleukin-1betaInterleukin-6NF-kappa BPtgs2 protein, mouseTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID27070323
PMCPMC4829159
OpenAlexW2337933193

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.