ArticleiScience2023
Adiponectin-mediated promotion of CD44 suppresses diabetic vascular inflammatory effects.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Adiponectin Inhibits AURKA to Suppress Inflammation in TNF-α-induced Keratinocytes and Attenuates Psoriatic Dermatitis in Mice.Immunity, inflammation and disease · 2026Article
- Reshaping the chromatin landscape in HUVECs from small-for-gestational-age newborns.JCI insight · 2025Article
- New advances of adiponectin in regulating obesity and related metabolic syndromes.Journal of pharmaceutical analysis · 2024Review
- Contents of exosomes derived from adipose tissue and their regulation on inflammation, tumors, and diabetes.Frontiers in endocrinology · 2024Review
- Effects of a Sodium-Glucose Cotransporter 2 Inhibitor Dapagliflozin on Pancreas in Obese Diabetic Mice.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While adiponectin (APN) was known to significantly abolish the diabetic endothelial inflammatory response, the specific mechanisms have yet to be elucidated. Aortic vascular tissues from mice fed normal and high-fat diets (HFD) were analyzed by transcriptome analysis. GO functional annotation showed that APN inhibited vascular endothelial inflammation in an APPL1-dependent manner. We confirmed that activation of the Wnt/β-catenin signaling plays a key role in APN-mediated anti-inflammation. Mechanistically, APN promoted APPL1/reptin complex formation and β-catenin nuclear translocation. Simultaneously, we identified APN promoted the expression of CD44 by activating TCF/LEF in an APPL1-mediated manner. Clinically, the serum levels of APN and CD44 were decreased in diabetes; the levels of these two proteins were positively correlated. Functionally, treatment with CD44 C-terminal polypeptides protected diabetes-induced vascular endothelial inflammation
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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.