ArticleDrug design, development and therapy2018
Icariside II ameliorates endothelial dysfunction by regulating the MAPK pathway via miR-126/SPRED1 in diabetic human cavernous endothelial cells.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Potential diagnostic value of microRNAs in vascular complications of diabetes: A systematic review and meta-analysis.Journal of endocrinological investigation · 2025Pooled it
- Downregulation of SPRED1 drives keratinocyte hyperproliferation in psoriasis via activation of the ERK-RSK1 signaling axis.iScience · 2026Article
- A comprehensive narrative review ofJournal of pharmaceutical analysis · 2026Review
- Pharmacological and Therapeutic Potential of a Natural Flavonoid Icariside II in Human Complication.Current drug targets · 2025Review
- A cellular regulator of the niche: telocyte.Tissue barriers · 2023Review
- microRNAs Control Antiviral Immune Response, Cell Death and Chemotaxis Pathways in Human Neuronal Precursor Cells (NPCs) during Zika Virus Infection.International journal of molecular sciences · 2022Article
- Expression of whole blood miR-126-3p, -30a-5p, -1299, -182-5p and -30e-3p in chronic kidney disease in a South African community-based sample.Scientific reports · 2022Article
- ICA II Alleviates Testicular Torsion Injury by Dampening the Oxidative and Inflammatory Stress.Frontiers in endocrinology · 2022Article
- Icariside Ⅱ Attenuates Palmitic Acid-Induced Endothelial Dysfunction Through SRPK1-Akt-eNOS Signaling Pathway.Frontiers in pharmacology · 2022Article
- Review
- LncRNA MALAT1 Promotes OGD-Induced Apoptosis of Brain Microvascular Endothelial Cells by Sponging miR-126 to Repress PI3K/Akt Signaling Pathway.Neurochemical research · 2020Article
- Article
- Epigenetic Regulation of miRNA Expression in Malignant Mesothelioma: miRNAs as Biomarkers of Early Diagnosis and Therapy.Frontiers in oncology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe aim of the study was to investigate whether miR-126, a regulator of MAPK signaling via targeting sprouty-related EVH1 domain-containing protein 1 ( MATERIALS AND
methodsPrimary hCECs were isolated and divided into three groups, normal control, diabetes mellitus (DM), and DM treated with ICA II. The cell proliferation and migration abilities of the hCECs were examined. The expression levels of endothelial-related microRNAs and relative target mRNAs (
resultshCECs induced with glucose plus advanced glycation end product-BSA showed a significant decrease in endothelial nitric oxide synthase, Ki-67, and miR-126 expression; a downregulated cell migration ability and an increased receptor for advanced glycation end products level. ICA II could partially reverse these changes.
conclusionICA II could ameliorate endothelial dysfunction by regulating the MAPK pathway via miR-126/SPRED1 in hCECs exposed to a diabetic-like environment, and ICA II might be a protective agent for endothelial function in diabetic ED.
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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.