Evidence map›Paper›PMID 16267791›Full record

ReviewHistology and histopathology2006

Winding through the WNT pathway during cellular development and demise.

F Li, Z Z Chong, K Maiese

Open access · greenAbstract readReview
In one paragraph

Review in Histology and histopathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

96 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. An Overview of Adverse Outcome Pathway Links between PMEnvironment & health (Washington, D.C.) · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Unlocking cardiomyocyte renewal potential for myocardial regeneration therapy.Journal of molecular and cellular cardiology · 2023
    Review
  10. Review
  11. Review
  12. Effect of Secreted Frizzled-Related Protein 5 in Mice with Heart Failure.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

36 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

F LiDivision of Cellular and Molecular Cerebral Ischemia, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
Z Z Chong
K Maiese
Wayne State University · US

Funding

RESEARCH CORE-- SIGNAL TRANSDUCTIONP30ES006639 · NIEHS · WAYNE STATE UNIVERSITY · PI RUNGE-MORRIS, MELISSA A · 1994 to 2008
$13.1M
Impacting Oxidative Stress and Cell Injury through Novel Pathways of the Wnt GeneR01NS053946 · NINDS · WAYNE STATE UNIVERSITY · PI MAIESE, KENNETH · 2007 to 2011
$2.4M
NIEHS NIH HHS P30 ES006639NIEHS NIH HHS P30 ES06639NINDS NIH HHS R01 NS053946
6 · The paper itself

Abstract

In slightly over a period of twenty years, our comprehension of the cellular and molecular mechanisms that govern the Wnt signaling pathway continue to unfold. The Wnt proteins were initially implicated in viral carcinogenesis experiments associated with mammary tumors, but since this period investigations focusing on the Wnt pathways and their transmembrane receptors termed Frizzled have been advanced to demonstrate the critical nature of Wnt for the development of a variety of cell populations as well as the potential of the Wnt pathway to avert apoptotic injury. In particular, Wnt signaling plays a significant role in both the cardiovascular and nervous systems during embryonic cell patterning, proliferation, differentiation, and orientation. Furthermore, modulation of Wnt signaling under specific cellular influences can either promote or prevent the early and late stages of apoptotic cellular injury in neurons, endothelial cells, vascular smooth muscle cells, and cardiomyocytes. A number of downstream signal transduction pathways can mediate the biological response of the Wnt proteins that include Dishevelled, beta-catenin, intracellular calcium, protein kinase C, Akt, and glycogen synthase kinase-3beta. Interestingly, these cellular cascades of the Wnt-Frizzled pathways can participate in several neurodegenerative, vascular, and cardiac disorders and may be closely integrated with the function of trophic factors. Identification of the critical elements that modulate the Wnt-Frizzled signaling pathway should continue to unlock the potential of Wnt pathway for the development of new therapeutic options against neurodegenerative and vascular diseases.

Indexed as

ApoptosisCell DifferentiationAnimalsCardiovascular DiseasesCardiovascular Physiological PhenomenaCardiovascular SystemFrizzled ReceptorsHumansNervous SystemNervous System Physiological PhenomenaNeurodegenerative DiseasesNeuronsSignal TransductionWnt ProteinsFrizzled ReceptorsWnt Proteins

Identifiers

PMID16267791
PMCPMC2247407
OpenAlexW1643634019

What OpenQuestion holds

Textmetadata
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.