Observational studyAngiogenesis2018
Antiangiogenesis and medical therapy failure in intracranial atherosclerosis.
Observational study in Angiogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 41 citations in OpenAlex.
- Endothelial progenitor cells-derived exosomes reduce ferroptosis and promote neovascularization after intracranial atherosclerosis in association with the NCOA4/FTH1 cascade modulation.Drug delivery and translational research · 2026Article
- Assessment of stress hyperglycemia ratio to predict all-cause mortality in patients with critical cerebrovascular disease: a retrospective cohort study from the MIMIC-IV database.Cardiovascular diabetology · 2025Article
- Hippo/YAP signaling pathway: a new therapeutic target for diabetes mellitus and vascular complications.Therapeutic advances in endocrinology and metabolism · 2023Review
- FOXG1 improves mitochondrial function and promotes the progression of nasopharyngeal carcinoma.Molecular medicine reports · 2021Article
- Oncolytic Virotherapy: From Bench to Bedside.Frontiers in cell and developmental biology · 2021Review
- Differential expression of circulating exosomal microRNAs in refractory intracranial atherosclerosis associated with antiangiogenesis.Scientific reports · 2019Article
- Inhibitory effect of melatonin on Mst1 ameliorates myocarditis through attenuating ER stress and mitochondrial dysfunction.Journal of molecular histology · 2019Article
- Article
- Mitofusin-2 regulates inflammation-mediated mouse neuroblastoma N2a cells dysfunction and endoplasmic reticulum stress via the Yap-Hippo pathway.The journal of physiological sciences : JPS · 2019Article
- Hippo/Mst1 overexpression induces mitochondrial death in head and neck squamous cell carcinoma via activating β-catenin/Drp1 pathway.Cell stress & chaperones · 2019Article
- Mammalian STE20-like Kinase 1 Knockdown Attenuates TNFα-Mediated Neurodegenerative Disease by Repressing the JNK Pathway and Mitochondrial Stress.Neurochemical research · 2019Article
- Irisin ameliorates septic cardiomyopathy via inhibiting DRP1-related mitochondrial fission and normalizing the JNK-LATS2 signaling pathway.Cell stress & chaperones · 2019Article
- Melatonin ameliorates endoplasmic reticulum stress in N2a neuroblastoma cell hypoxia-reoxygenation injury by activating the AMPK-Pak2 pathway.Cell stress & chaperones · 2019Article
- Sirtuin 3 inhibition induces mitochondrial stress in tongue cancer by targeting mitochondrial fission and the JNK-Fis1 biological axis.Cell stress & chaperones · 2019Article
- Differential Expression of Vascular Endothelial Growth Factor-AJournal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2019Article
- Mst1 overexpression combined with Yap knockdown augments thyroid carcinoma apoptosis via promoting MIEF1-related mitochondrial fission and activating the JNK pathway.Cancer cell international · 2019Article
- Large tumor suppressor kinase 2 overexpression attenuates 5-FU-resistance in colorectal cancer via activating the JNK-MIEF1-mitochondrial division pathway.Cancer cell international · 2019Article
- Genetic ablation of TAZ induces HepG2 liver cancer cell apoptosis through activating the CaMKII/MIEF1 signaling pathway.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Intracranial atherosclerotic disease (ICAD) is one of the most common causes of stroke worldwide and the one with the worst prognosis. In this study, we assessed the hypothesis that the balance of circulating pro- and antiangiogenic factors plays a role in the evolution of the disease and can be used as a potential marker for the disease course and a target for treatment. Seventy-four patients with severe ICAD were enrolled in this prospective observational study, medically optimized, and followed for 6 months. Thirteen pro- and eight antiangiogenic factors were measured in the participants' serum using a sandwich multiplex ELISA. Angiogenic profiles were calculated using principal component analysis. We tested the association between angiogenic profiles and recurring cerebrovascular events despite intensive medical therapy, disability at 6 months after enrollment, and angiographic neovascularization in patients who failed medical treatment and underwent indirect revascularization surgery. There is a strong association between a functionally antiangiogenic profile and recurrent stroke or TIA in patients with ICAD (OR = 7.2, CI 2.4-34.4). Multivariable regression analysis showed that this antiangiogenic profile was also associated with poor functional status after 6 months (p = 0.002), independent from other clinical features such as history of previous stroke, diabetes, and age. In patients who failed medical management and underwent indirect revascularization surgery, high endostatin and angiostatin levels were also associated with low angiographic neovascularization (p = 0.02). The results of this study point to the striking importance of antiangiogenesis as a determinant of ICAD patient prognosis and suggest a possible new target for therapy.
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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.