ArticleClinical and translational medicine2020
CD248 as a novel therapeutic target in pulmonary arterial hypertension.
Article in Clinical and translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- New Drugs and Therapies in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension.Molecules (Basel, Switzerland) · 2022Review
- Regulation of the Methylation and Expression Levels of the BMPR2 Gene by SIN3a as a Novel Therapeutic Mechanism in Pulmonary Arterial Hypertension.Circulation · 2021Article
- Retraction: CD248 as a novel therapeutic target in pulmonary arterial hypertension.Clinical and translational medicine · 2021Article
- Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus.Bioscience reports · 2021Article
- A Novel Resveratrol Analog Upregulates SIRT1 Expression and Ameliorates Neointima Formation.Frontiers in cardiovascular medicine · 2021Article
- CD248 as a novel therapeutic target in pulmonary arterial hypertension.Clinical and translational medicine · 2020Article
Corrections and comments
- Retraction · 2021-07-16Duplication of Data · Duplication of/in Image ·
- Retracted
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary vascular remodeling is the most important pathological characteristic of pulmonary arterial hypertension (PAH). No effective treatment for PAH is currently available because the mechanism underlying vascular remodeling is not completely clear. CD248, also known as endosialin, is a transmembrane protein that is highly expressed in pericytes and fibroblasts. Here, we evaluated the role of CD248 in pulmonary vascular remodeling and the processes of PAH pathogenesis. Activation of CD248 in pulmonary artery smooth muscle cells (PASMCs) was found to be proportional to the severity of PAH. CD248 contributed to platelet-derived growth factor-BB (PDGF-BB)-induced PASMC proliferation and migration along with the shift to more synthetic phenotypes. In contrast, treatment with Cd248 siRNA or the anti-CD248 therapeutic antibody (ontuxizumab) significantly inhibited the PDGF signaling pathway, obstructed NF-κB p65-mediated transcription of Nox4, and decreased reactive oxygen species production induced by PDGF-BB in PAMSCs. In addition, knockdown of CD248 alleviated pulmonary vascular remodeling in rat PAH models. This study provides novel insights into the dysfunction of PASMCs leading to pulmonary vascular remodeling, and provides evidence for anti-remodeling treatment for PAH via the immediate targeting of CD248.
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.