Evidence map›Paper›PMID 18432188›Full record

ArticleKidney international2008

Common genetic variants in the chromogranin A promoter alter autonomic activity and blood pressure.

Y Chen, F Rao, J L Rodriguez-Flores, N R Mahapatra, M Mahata, G Wen, R M Salem, P-A B Shih, M Das, N J Schork and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Kidney international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. A haplotype variant of the human chromogranin A gene (The Journal of biological chemistry · 2017
    Article
  6. Article
  7. Article
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  10. Article
  11. Review
  12. Article
  13. Article
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  15. Article
  16. Article
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  18. Article
  19. Article
  20. Chromogranin A: a novel susceptibility gene for essential hypertension.Cellular and molecular life sciences : CMLS · 2010
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Y ChenDepartment of Medicine, Center for Human Genetics and Genomics, University of California at San Diego, San Diego, California 92093-0838, USA.
F Rao
J L Rodriguez-Flores
N R Mahapatra
M Mahata
G Wen
R M Salem
P-A B Shih
M Das
N J Schork
M G Ziegler
B A Hamilton
S K Mahata
D T O'Connor
Center for Human Genetics · USUniversity of California, San Diego · US

Funding

Trafficking of catecholamine storage vesicle proteinsP01HL058120 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZIEGLER, MICHAEL G. · 1999 to 2009
$18.5M
Sympathetic Outflow to Catecholamine Storage VesiclesR01DK060702 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI O'CONNOR, DANIEL T · 2002 to 2006
$1.4M
NHLBI NIH HHS P01 HL058120NIDDK NIH HHS R01 DK060702
6 · The paper itself

Abstract

Chromogranin A (CHGA) is stored and released from the same secretory vesicles that contain catecholamines in chromaffin cells and noradrenergic neurons. We had previously identified common genetic variants at the CHGA locus in several human populations. Here we focus on whether inter-individual variants in the promoter region are of physiological significance. A common haplotype, CGATA (Hap-B), blunted the blood pressure response to cold stress and the effect exhibited molecular heterosis with the greatest blood pressure change found in Hap-A/Hap-B heterozygotes. Homozygosity for three minor alleles with peak effects within the haplotype predicted lower stress-induced blood pressure changes. The G-462A variant predicted resting blood pressure in the population with higher pressures occurring in heterozygotes (heterosis). Using cells transfected with CHGA promoter-luciferase reporter constructs, the Hap-B haplotype had decreased luciferase expression compared to the TTGTC (Hap-A) haplotype under both basal conditions and after activation by pre-ganglionic stimuli. The G-462A variant altered a COUP-TF transcriptional control motif. The two alleles in transfected promoters differed in basal activity and in the responses to COUP-II-TF transactivation and to retinoic acid. In vitro findings of molecular heterosis were also noted with the transfected CHGA promoter wherein the diploid combination of the two G-462A alleles gave rise to higher luciferase expression than either allele in isolation. Our results suggest that common genetic variants in the CHGA promoter may regulate heritable changes in blood pressure.

Indexed as

Polymorphism, Single NucleotideAdaptation, PhysiologicalAutonomic Nervous SystemBlood PressureChromogranin AGenotypeHaplotypesHumansLinkage DisequilibriumPromoter Regions, GeneticChromogranin A

Identifiers

PMID18432188
PMCPMC2576285
OpenAlexW2029184704

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.