Evidence map›Paper›PMID 21826523›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2012

Molecular mechanisms underlying cardiac antihypertrophic and antifibrotic effects of natriuretic peptides.

Camilla Calvieri, Speranza Rubattu, Massimo Volpe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 77 citations in OpenAlex.

  1. Trial
  2. Cardiac Biomarkers in Chronic Kidney Disease: Signal or Noise?Clinical journal of the American Society of Nephrology : CJASN · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Role of Cardiac Natriuretic Peptides in Heart Structure and Function.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Pseudomonas aeruginosa Biofilm Dispersion by the Human Atrial Natriuretic Peptide.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  14. Targeting Cyclic Guanylate Monophosphate in Resistant Hypertension and Heart Failure: Are Sacubitril/Valsartan and Vericiguat Synergistic and Effective in Both Conditions?High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2021
    Article
  15. Review
  16. cGMP Signaling and Modulation in Heart Failure.Journal of cardiovascular pharmacology · 2020
    Review
  17. Review
  18. Review
  19. Article
  20. Cardiovascular Pleiotropic Effects of Natriuretic Peptides.International journal of molecular sciences · 2019
    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

3 authors at 2 institutions in 1 country.

Camilla CalvieriCardiology, Department of Clinical and Molecular Medicine, School of Medicine and Psychology, University Sapienza of Rome, Ospedale S. Andrea, Rome, Italy.
Speranza Rubattu
Massimo Volpe
Sapienza University of Rome · ITAzienda Ospedaliera Sant'Andrea · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natriuretic peptides (NPs) exert well-characterized protective effects on the cardiovascular system, such as vasorelaxation, natri- and diuresis, increase of endothelial permeability, and inhibition of renin-angiotensin-aldosterone system. It has been reported that they also possess antihypertrophic and antifibrotic properties and contribute actively to cardiac remodeling. As a consequence, they are involved in several aspects of cardiovascular diseases. Antihypertrophic and antifibrotic actions of NPs appear to be mediated by specific signaling pathways within a more complex cellular network. Elucidation of the molecular mechanisms underlying the effects of NPs on cardiac remodeling represents an important research objective in order to gain more insights on the complex network leading to cardiac hypertrophy, ventricular dysfunction, and transition to heart failure, and in the attempt to develop novel therapeutic agents. The aim of the present article is to review well-characterized molecular mechanisms underlying the antihypertrophic and antifibrotic effects of NPs in the heart that appear to be mainly mediated by guanylyl cyclase type A receptor. In particular, we discuss the calcineurin/NFAT, the sodium exchanger NHE-1, and the TGFβ1/Smad signaling pathways. The role of guanylyl cyclase type B receptor, along with the emerging functional significance of natriuretic peptide receptor type C as mediators of CNP antihypertrophic and antifibrotic actions in the heart are also considered.

Indexed as

AnimalsCalcineurinCardiomegalyFibrosisHumansMyocardiumNatriuretic Peptide, C-TypeNatriuretic PeptidesNFATC Transcription FactorsSignal TransductionSmad ProteinsSodium-Hydrogen ExchangersTransforming Growth Factor beta1Calcineuringrowth factor-activatable Na-H exchanger NHE-1Natriuretic Peptide, C-TypeNatriuretic PeptidesNFATC Transcription FactorsSmad ProteinsSodium-Hydrogen ExchangersTransforming Growth Factor beta1

Identifiers

PMID21826523
OpenAlexW2151737394

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.