Evidence map›Paper›PMID 25651559›Full record

ReviewAmerican journal of physiology. Renal physiology2015

ANP-induced signaling cascade and its implications in renal pathophysiology.

Franziska Theilig, Qingyu Wu

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

Review in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.5field-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

67 citing papers in PubMed, 110 citations in OpenAlex.

  1. Trial
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  10. Observational
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  16. Review
  17. Review
  18. Low plasma renin activity is associated with "Apparently" idiopathic atrial fibrillation.International journal of cardiology. Heart & vasculature · 2023
    Article
  19. Article
  20. Natriuretic Peptide Signaling in Uterine Biology and Preeclampsia.International journal of molecular sciences · 2023
    Review

7 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Franziska TheiligInstitute of Anatomy, Department of Medicine, University of Fribourg, Fribourg, Switzerland; and franziska.theilig@unifr.ch.
Qingyu WuMolecular Cardiology, Lerner Research Institute, Cleveland Clinic, Ohio.
Cleveland Clinic Lerner College of Medicine · USUniversity of Fribourg · CH

Funding

The cardiac protease corin in natriuretic peptide processing and hypertensionR01HL089298 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI WU, QINGYU · 2008 to 2012
$2.2M
Serine Protease Corin in Pregnancy-induced HypertensionR01HD064634 · NICHD · CLEVELAND CLINIC LERNER COM-CWRU · PI WU, QINGYU · 2011 to 2015
$1.6M
NHLBI NIH HHS HL089298NICHD NIH HHS HD064634NICHD NIH HHS R01 HD064634
6 · The paper itself

Abstract

The balance between vasoconstrictor/sodium-retaining and vasodilator/natriuretic systems is essential for maintaining body fluid and electrolyte homeostasis. Natriuretic peptides, such as atrial natriuretic peptide (ANP), belong to the vasodilator/natriuretic system. ANP is produced by the conversion of pro-ANP into ANP, which is achieved by a proteolytical cleavage executed by corin. In the kidney, ANP binds to the natriuretic peptide receptor-A (NPR-A) and enhances its guanylyl cyclase activity, thereby increasing intracellular cyclic guanosine monophosphate production to promote natriuretic and renoprotective responses. In the glomerulus, ANP increases glomerular permeability and filtration rate and antagonizes the deleterious effects of the renin-angiotensin-aldosterone system activation. Along the nephron, natriuretic and diuretic actions of ANP are mediated by inhibiting the basolaterally expressed Na(+)-K(+)-ATPase, reducing apical sodium, potassium, and protein organic cation transporter in the proximal tubule, and decreasing Na(+)-K(+)-2Cl(-) cotransporter activity and renal concentration efficiency in the thick ascending limb. In the medullary collecting duct, ANP reduces sodium reabsorption by inhibiting the cyclic nucleotide-gated cation channels, the epithelial sodium channel, and the heteromeric channel transient receptor potential-vanilloid 4 and -polycystin 2 and diminishes vasopressin-induced water reabsorption. Long-term ANP treatment may lead to NPR-A desensitization and ANP resistance, resulting in augmented sodium and water reabsorption. In mice, corin deficiency impairs sodium excretion and causes salt-sensitive hypertension. Characteristics of ANP resistance and corin deficiency are also encountered in patients with edema-associated diseases, highlighting the importance of ANP signaling in salt-water balance and renal pathophysiology.

Indexed as

AnimalsAtrial Natriuretic FactorGlomerular Filtration RateHumansKidneyMiceModels, AnimalSerine EndopeptidasesSignal TransductionWater-Electrolyte BalanceAtrial Natriuretic FactorCORIN protein, humanCorin protein, mouseSerine EndopeptidasesANPcorinedemavolume retention

Identifiers

PMID25651559
PMCPMC4436998
OpenAlexW2019457908

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.