Evidence map›Paper›PMID 40383495›Full record

ArticleVascular pharmacology2025

Pharmacological activation of NO-sensitive guanylyl cyclase ameliorates obesity-induced arterial stiffness.

Enkhjargal Budbazar, Aylin Balmes, Danielle Elliott, Lisette Peres Tintin, Timo Kopp, Susanne Feil, Robert Feil, Tilman E Schäffer, Francesca Seta

Abstract read
In one paragraph

Article in Vascular pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. CNP-induced cGMP signaling reduces growth cone stiffness and CaFrontiers in molecular neuroscience · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Enkhjargal BudbazarVascular Biology Section, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, USA.
Aylin BalmesInstitute of Applied Physics, University of Tübingen, Germany.
Danielle ElliottVascular Biology Section, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, USA.
Lisette Peres TintinVascular Biology Section, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, USA.
Timo KoppInterfaculty Institute of Biochemistry, University of Tübingen, Germany.
Susanne FeilInterfaculty Institute of Biochemistry, University of Tübingen, Germany.
Robert FeilInterfaculty Institute of Biochemistry, University of Tübingen, Germany.
Tilman E SchäfferInstitute of Applied Physics, University of Tübingen, Germany.
Francesca SetaVascular Biology Section, Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, USA. Electronic address: setaf@bu.edu.

Funding

Project-005UL1TR001430 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BAIR-MERRITT, MEGAN H, CENTER, DAVID M. · 2015 to 2024
$52.3M
The role of Bcl11b in dementia associated with Parkinsons diseaseR01HL136311 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SETA, FRANCESCA · 2018 to 2022
$2.8M
NCATS NIH HHS UL1 TR001430NHLBI NIH HHS R01 HL136311
6 · The paper itself

Abstract

BACKGROUND & PURPOSE: Arterial stiffness, or loss of elastic compliance in large arteries, is an independent precursor of cardiovascular disease (CVD) [1] and dementia [2] for which currently there are no targeted therapies. We previously discovered that decreases in NO-sensitive guanylyl cyclase (NO-GC), the NO receptor which synthesizes cGMP, and in its target vasodilator-stimulated phosphoprotein (pVASP EXPERIMENTAL APPROACH & KEY

resultsCinaciguat administration (5 mg/kg) to high fat, high sucrose diet (HFHS)-fed mice, our established model of arterial stiffness [4], (1) decreased pulse wave velocity, the in vivo index of arterial stiffness, without affecting blood pressure; (2) increased aortic pVASP CONCLUSIONS & IMPLICATIONS: Collectively, our data strongly support the notion that pharmacological NO-GC activation would be beneficial in decreasing obesity-associated arterial stiffness by decreasing VSMC cytoskeletal actin hyper-polymerization. If translated to humans, NO-GC activators could become a viable approach to clinically treat arterial stiffness, which remains an unmet medical need.

Indexed as

Enzyme ActivatorsGuanylate CyclaseMuscle, Smooth, VascularMyocytes, Smooth MuscleObesityVascular StiffnessActinsAnimalsCell Adhesion MoleculesCells, CulturedDiet, High-FatDisease Models, AnimalEnzyme ActivationMaleMiceMice, Inbred C57BLActinsCell Adhesion MoleculesEnzyme ActivatorsGuanylate CyclaseMicrofilament ProteinsVasodilator-Stimulated PhosphoproteinActin polymerizationArterial stiffnessCinaciguatNO-sensitive guanylyl cyclase activatorsVascular smooth muscle cells

Identifiers

PMID40383495
PMCPMC12186992

What OpenQuestion holds

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Registered trials

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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.