Evidence map›Paper›PMID 32216738›Full record

ReviewCurrent neurovascular research2020

Prospects and Perspectives for WISP1 (CCN4) in Diabetes Mellitus.

Kenneth Maiese

Open access · hybridAbstract readReview
In one paragraph

Review in Current neurovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Knockdown of WISP1/DKK1 restrains phenotypic plasticity in esophageal squamous cell carcinoma by suppressing epithelial-mesenchymal transition and stemness.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. An overview of CCN4 (WISP1) role in human diseases.Journal of translational medicine · 2024
    Review
  12. Article
  13. Review
  14. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
    Review
  15. CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review
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

1 author.

Kenneth MaieseCellular and Molecular Signaling, New York, NY 10022, United States.

Funding

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
NINDS NIH HHS R01 NS053946
6 · The paper itself

Abstract

The prevalence of diabetes mellitus (DM) continues to increase throughout the world. In the United States (US) alone, approximately ten percent of the population is diagnosed with DM and another thirty-five percent of the population is considered to have prediabetes. Yet, current treatments for DM are limited and can fail to block the progression of multi-organ failure over time. Wnt1 inducible signaling pathway protein 1 (WISP1), also known as CCN4, is a matricellular protein that offers exceptional promise to address underlying disease progression and develop innovative therapies for DM. WISP1 holds an intricate relationship with other primary pathways of metabolism that include protein kinase B (Akt), mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), and mammalian forkhead transcription factors (FoxOs). WISP1 is an exciting prospect to foster vascular as well as neuronal cellular protection and regeneration, control cellular senescence, block oxidative stress injury, and maintain glucose homeostasis. However, under some scenarios WISP1 can promote tumorigenesis, lead to obesity progression with adipocyte hyperplasia, foster fibrotic hepatic disease, and lead to dysregulated inflammation with the progression of DM. Given these considerations, it is imperative to further elucidate the complex relationship WISP1 holds with other vital metabolic pathways to successfully develop WISP1 as a clinically effective target for DM and metabolic disorders.

Indexed as

AnimalsCCN Intercellular Signaling ProteinsDiabetes MellitusHumansHypoglycemic AgentsMetabolic Networks and PathwaysProto-Oncogene ProteinsCCN4 protein, humanCCN Intercellular Signaling ProteinsHypoglycemic AgentsProto-Oncogene ProteinsAktAMP activated protein kinase (AMPK)autophagycancerCCN4diabetes mellitusforkhead transcription factorsFoxOinflammationinterleukin 18 (IL-18)mechanistic target of rapamycin (mTOR)oxidative stresssilent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1)sirtuinstem cellswinglessWISP-1WntWnt1 inducible signaling pathway protein 1 (WISP1)

Identifiers

PMID32216738
PMCPMC7529678
OpenAlexW3013402956

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.