Evidence map›Paper›PMID 30169131›Full record

ReviewPhysiological genomics2018

Molecular and genetic aspects of guanylyl cyclase natriuretic peptide receptor-A in regulation of blood pressure and renal function.

Kailash N Pandey

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Physiological genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Podocyte cell-specificPhysiological genomics · 2024
    Article
  3. Epigenetic mechanisms differentially regulate blood pressure and renal dysfunction in male and female Npr1 haplotype mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Discovery of small molecule guanylyl cyclase A receptor positive allosteric modulators.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Review
  18. Article
  19. Observational
  20. Cardiac natriuretic peptides.Nature reviews. Cardiology · 2020
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Kailash N PandeyDepartment of Physiology, Tulane University Health Sciences Center, School of Medicine , New Orleans, Louisiana.
Tulane University · US

Funding

Study of ANP Receptor: Gene Targeting and ExpressionR01HL062147 · TULANE UNIVERSITY OF LOUISIANA · 1998 to 2005
$984k
ANP RECEPTOR--MOLECULAR APPROACH OF SIGNALING MECHANISMSR01HL057531 · TULANE UNIVERSITY OF LOUISIANA · 1997 to 2005
$891k
NHLBI NIH HHS R01 HL057531NHLBI NIH HHS R01 HL062147
6 · The paper itself

Abstract

Natriuretic peptides (NPs) exert diverse effects on several biological and physiological systems, such as kidney function, neural and endocrine signaling, energy metabolism, and cardiovascular function, playing pivotal roles in the regulation of blood pressure (BP) and cardiac and vascular homeostasis. NPs are collectively known as anti-hypertensive hormones and their main functions are directed toward eliciting natriuretic/diuretic, vasorelaxant, anti-proliferative, anti-inflammatory, and anti-hypertrophic effects, thereby, regulating the fluid volume, BP, and renal and cardiovascular conditions. Interactions of NPs with their cognate receptors display a central role in all aspects of cellular, biochemical, and molecular mechanisms that govern physiology and pathophysiology of BP and cardiovascular events. Among the NPs atrial and brain natriuretic peptides (ANP and BNP) activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) and initiate intracellular signaling. The genetic disruption of Npr1 (encoding GC-A/NPRA) in mice exhibits high BP and hypertensive heart disease that is seen in untreated hypertensive subjects, including high BP and heart failure. There has been a surge of interest in the NPs and their receptors and a wealth of information have emerged in the last four decades, including molecular structure, signaling mechanisms, altered phenotypic characterization of transgenic and gene-targeted animal models, and genetic analyses in humans. The major goal of the present review is to emphasize and summarize the critical findings and recent discoveries regarding the molecular and genetic regulation of NPs, physiological metabolic functions, and the signaling of receptor GC-A/NPRA with emphasis on the BP regulation and renal and cardiovascular disorders.

Indexed as

AnimalsAtrial Natriuretic FactorBlood PressureCardiovascular DiseasesDiabetes ComplicationsHepatitisHumansHypertensionKidneyMiceNatriuretic Peptide, C-TypePolymorphism, GeneticProtein PrecursorsReceptors, Atrial Natriuretic FactorRenin-Angiotensin SystemSodiumAtrial Natriuretic Factoratrial natriuretic factor receptor ANatriuretic Peptide, C-TypeNPPA protein, humanNppa protein, mouseProtein PrecursorsReceptors, Atrial Natriuretic FactorSodiumcardiovascular hemostasiscGMPgene-targetinghypertensionnatriuretic peptide receptorreceptor signaling

Identifiers

PMID30169131
PMCPMC6293115
OpenAlexW2888884176

What Socratic 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 Socratic graph.