ArticleFuture cardiology2008
Role of fetal programming in the development of hypertension.
Article in Future cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed, 14 citations in OpenAlex.
- Stereological and histopathological assessment of intrauterine growth restriction placenta from Saudi women.Saudi journal of biological sciences · 2023Article
- Differential restoration of functional hyperemia by antihypertensive drug classes in hypertension-related cerebral small vessel disease.The Journal of clinical investigation · 2021Article
- Whole transcriptome analysis of adrenal glands from prenatal glucocorticoid programmed hypertensive rodents.Scientific reports · 2020Article
- Modularity/non-cumulativity of quantitative trait loci on blood pressure.Journal of human hypertension · 2020Review
- Conserved mammalian modularity of quantitative trait loci revealed human functional orthologs in blood pressure control.PloS one · 2020Article
- Prenatal dexamethasone and postnatal high-fat diet have a synergistic effect of elevating blood pressure through a distinct programming mechanism of systemic and adipose renin-angiotensin systems.Lipids in health and disease · 2018Article
- Increased renal apoptosis and reduced renin-angiotensin system in fetal growth restriction.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiological studies have suggested that size at birth contributes to increased cardiovascular disease (CVD) risk in later life. Findings from experimental studies are providing insight into the mechanisms linking impaired fetal growth and the increased risk of CVD and hypertension in adulthood. This article summarizes potential mechanisms involved in the fetal programming of hypertension and CVD, including alterations in the organs and regulatory systems critical to long-term control of sodium and volume homeostasis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.