ArticleBMC medical genetics2013
Contribution of SLC7A1 genetic variant to hypertension, the TAMRISK study.
Article in BMC medical genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- Precision formulation, a new concept to improve dietary amino acid absorption based on the study of cationic amino acid transporters.iScience · 2024Article
- Transport of L-Arginine Related Cardiovascular Risk Markers.Journal of clinical medicine · 2020Review
- Lack of family-based association between common variations in WNK1 and blood pressure level.Medical science monitor : international medical journal of experimental and clinical research · 2014Article
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
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe rs41318021 polymorphism in the SLC7A1 gene affects endothelial NO production through changes in L-arginine transport. This variation could thus hypothetically cause dysfunction of endothelium and lead to hypertension. The association of rs41318021 with hypertension was therefore studied in a Finnish cohort.
methodsA total of 412 hypertensive cases and 771 non-hypertensive controls from a Finnish 50-year-old cohort were included in this study. The data was collected from the Tampere adult population cardiovascular risk study (TAMRISK). DNA was extracted from buccal swabs and amplified using PCR. A subpopulation of men and women who had available follow-up data of blood pressure measurements at the age of 35-, 40-, 45- and 50 years was also analyzed.
resultsThere was no difference between the variant frequencies of the hypertension group and normotensive group at the age of 50 years (p = 0.209). However, repeated measures analysis from the 15-year follow-up showed that subjects having gene variants CT or TT had slightly higher diastolic blood pressure than subjects having genotype CC (p = 0.047). By post-hoc analysis, this was most pronounced at the age of 35 years (p = 0.044).
conclusionThe rs41318021 polymorphism in the SLC7A1 gene was not associated with essential hypertension in 50-year-old subjects. However, a borderline effect of this variation upon diastolic blood pressure was seen in these same subjects in a 15-year follow-up from a 35-year-old cohort to 50 years of age.
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.