ArticleJCI insight2018
Angiokine Wisp-1 is increased in myocardial infarction and regulates cardiac endothelial signaling.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- ANTXR1 blockade enhances cardiac function in preclinical models of heart failure.Nature cardiovascular research · 2025Article
- Recent advances of PIWI-interacting RNA in cardiovascular diseases.Clinical and translational medicine · 2024Review
- Pathophysiological pathways related to high plasma growth differentiation factor 15 concentrations in patients with heart failure.European journal of heart failure · 2022Article
- Activation of Frizzled-7 attenuates blood-brain barrier disruption through Dvl/β-catenin/WISP1 signaling pathway after intracerebral hemorrhage in mice.Fluids and barriers of the CNS · 2021Article
- Prevention of Fibrosis and Pathological Cardiac Remodeling by Salinomycin.Circulation research · 2021Article
- Autocrine Signaling in Cardiac Remodeling: A Rich Source of Therapeutic Targets.Journal of the American Heart Association · 2021Review
- An Update to the WISP-1/CCN4 Role in Obesity, Insulin Resistance and Diabetes.Medicina (Kaunas, Lithuania) · 2021Review
- Circulating levels of selected adipokines in women with gestational diabetes and type 2 diabetes.Journal of applied biomedicine · 2020Article
- Adipokines: New Potential Therapeutic Target for Obesity and Metabolic, Rheumatic, and Cardiovascular Diseases.Frontiers in physiology · 2020Review
- Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review.Frontiers in cell and developmental biology · 2020Review
- Prospects and Perspectives for WISP1 (CCN4) in Diabetes Mellitus.Current neurovascular research · 2020Review
- Article
- Aging Disrupts Muscle Stem Cell Function by Impairing Matricellular WISP1 Secretion from Fibro-Adipogenic Progenitors.Cell stem cell · 2019Article
- Wnt signaling pathways in myocardial infarction and the therapeutic effects of Wnt pathway inhibitors.Acta pharmacologica Sinica · 2019Review
- Sirtuins: Developing Innovative Treatments for Aged-Related Memory Loss and Alzheimer's Disease.Current neurovascular research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial infarctions (MIs) cause the loss of myocytes due to lack of sufficient oxygenation and latent revascularization. Although the administration of histone deacetylase (HDAC) inhibitors reduces the size of infarctions and improves cardiac physiology in small-animal models of MI injury, the cellular targets of the HDACs, which the drugs inhibit, are largely unspecified. Here, we show that WNT-inducible secreted protein-1 (Wisp-1), a matricellular protein that promotes angiogenesis in cancers as well as cell survival in isolated cardiac myocytes and neurons, is a target of HDACs. Further, Wisp-1 transcription is regulated by HDACs and can be modified by the HDAC inhibitor, suberanilohydroxamic acid (SAHA/vorinostat), after MI injury. We observe that, at 7 days after MI, Wisp-1 is elevated 3-fold greater in the border zone of infarction in mice that experience an MI injury and are injected daily with SAHA, relative to MI alone. Additionally, human coronary artery endothelial cells (HCAECs) produce WISP-1 and are responsive to autocrine WISP-1-mediated signaling, which functionally promotes their proangiogenic behavior. Altering endogenous expression of WISP-1 in HCAECs directly impacts their network density in vitro. Therapeutic interventions after a heart attack define the extent of infarct injury, cell survival, and overall prognosis. Our studies shown here identify a potentially novel cardiac angiokine, Wisp-1, that may contribute to beneficial post-MI treatment modalities.
Indexed as
Identifiers
What OpenQuestion holds
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.