Evidence map›Paper›PMID 39443532›Full record

ArticleScientific reports2024

Sacubitril/valsartan improves diastolic left ventricular stiffness with increased titin phosphorylation via cGMP-PKG activation in diabetic mice.

Nozomi Furukawa, Hiroki Matsui, Hiroaki Sunaga, Kohzo Nagata, Masaaki Hirayama, Hideru Obinata, Tomoyuki Yokoyama, Kinji Ohno, Masahiko Kurabayashi, Norimichi Koitabashi

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
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  3. Review
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  5. Article
  6. 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

10 authors.

Nozomi FurukawaDepartment of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroki MatsuiDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi, Japan.
Hiroaki SunagaDepartment of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22, Showa-Machi, Maebashi, Gunma, 371-8511, Japan.
Kohzo NagataDepartment of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masaaki HirayamaDepartment of Occupational Therapy, Chubu University College of Life and Health Sciences, Kasugai, Japan.
Hideru ObinataEducation and Research Support Center, Gunma University Graduate School of Medicine, Maebashi, Japan.
Tomoyuki YokoyamaDepartment of Laboratory Sciences, Gunma University Graduate School of Health Sciences, Maebashi, Japan.
Kinji OhnoGraduate School of Nutritional Sciences, Nagoya University of Arts and Sciences, Nisshin, Japan.
Masahiko KurabayashiDepartment of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22, Showa-Machi, Maebashi, Gunma, 371-8511, Japan.
Norimichi KoitabashiDepartment of Cardiovascular Medicine, Gunma University Graduate School of Medicine, 3-39-22, Showa-Machi, Maebashi, Gunma, 371-8511, Japan. koitabas@gunma-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Titin, a giant sarcomeric protein, regulates diastolic left ventricular (LV) passive stiffness as a molecular spring and could be a therapeutic target for diastolic dysfunction. Sacubitril/valsartan (Sac/Val), an angiotensin receptor neprilysin inhibitor, has been shown to benefit patients with heart failure with preserved ejection fraction. The effect of Sac/Val is thought to be due to the enhancement of the cGMP/PKG pathway via natriuretic peptide. In this study, the effects of Sac/Val on LV diastolic dysfunction are demonstrated in a mouse diabetic cardiomyopathy model focusing on titin phosphorylation. Sac/Val-treated diabetic mice showed a greater increase in myocardial levels of cGMP-PKG than Val-treated and control mice. Conductance catheter analysis showed a significant reduction in LV stiffness in diabetic mice, but not in non-diabetic mice. Notably, diastolic LV stiffness was significantly reduced in Sac/Val-treated diabetic hearts compared with Val-treated or vehicle-treated diabetic mice. The phosphorylation level of titin (N2B), which determines passive stiffness and modulates active contraction, was higher in Sac/Val-treated hearts compared with Val-treated hearts in diabetic mice. Given that alteration of titin phosphorylation through PKG contributes to myocardial stiffness, the beneficial effects of Sac/Val in heart failure might be partly attributed to the induction of titin phosphorylation.

Indexed as

AminobutyratesBiphenyl CompoundsConnectinCyclic GMPCyclic GMP-Dependent Protein KinasesDiabetes Mellitus, ExperimentalDrug CombinationsValsartanAngiotensin Receptor AntagonistsAnimalsDiabetic CardiomyopathiesDiastoleHeart VentriclesMaleMiceMice, Inbred C57BLAminobutyratesAngiotensin Receptor AntagonistsBiphenyl CompoundsConnectinCyclic GMPCyclic GMP-Dependent Protein KinasesDrug CombinationsProtein Kinasessacubitril and valsartan sodium hydrate drug combinationtitin protein, mouseValsartanCardiomyopathyDiabetesDiastolic dysfunctionHFpEFMyocardial stiffnessTitin

Identifiers

PMID39443532
PMCPMC11499646

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.