ArticleHypertension (Dallas, Tex. : 1979)2026
Inducible Endothelial
Article in Hypertension (Dallas, Tex. : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- FTO/m6A Regulate Prenatal Nicotine-Induced eNOS Uncoupling and BP Susceptibility.Hypertension (Dallas, Tex. : 1979) · 2026Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase. Constitutive endothelial BH4 deficiency leads to mild hypertension and vascular dysfunction that are partly compensated by alternative endothelium-derived vasodilators. Accordingly, we generated a novel VE-Cadherin-CreERT2 (VE-Cad-Cre) mouse to evaluate the impact of inducing endothelial-specific BH4 deficiency in adult animals, without the potential mitigating effects of developmental or other adaptive mechanisms.
methodsEndothelial
resultsMale and female
conclusionsInduction of endothelial cell BH4 deficiency reveals rapid, sex-specific requirements for endothelial cell BH4 in vascular function and blood pressure, and the cardiovascular response to pregnancy. These changes are more striking than those reported for constitutive endothelial cell BH4 deficiency, suggesting a role for developmental or other adaptive effects that fail to mitigate the effects of inducible endothelial cell BH4 deficiency. Targeting endothelial BH4 bioavailability may offer therapeutic strategies for acquired hypertensive disorders and fetal growth restriction.
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.