Evidence map›Paper›PMID 41155405›Full record

ArticleInternational journal of molecular sciences2025

Systemic Metabolic Rewiring in a Mouse Model of Left Ventricular Hypertrophy.

Alexandra V Schmidt, Tharika Thambidurai, Olivia D'Annibale, Sivakama S Bharathi, Tim Wood, Eric S Goetzman, Julian E Stelzer

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Alexandra V SchmidtDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.ORCID 0000-0002-9293-7786
Tharika ThambiduraiDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.
Olivia D'AnnibaleBiochemical Genetics Laboratory, Children's Hospital of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Sivakama S BharathiDepartment of Pediatrics, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15224, USA.ORCID 0000-0003-0611-2778
Tim WoodBiochemical Genetics Laboratory, Children's Hospital of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Eric S GoetzmanDepartment of Pediatrics, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15224, USA.
Julian E StelzerDepartment of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA.

Funding

Computer modeling of myosin binding protein C and its effects on cardiac contractionR01HL146676 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI Kenneth S Campbell, Julian Stelzer · 2019 to 2026
$4.3M
Novel downstream effectors of protein kinase G in hypertensive diseaseR01HL153236 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI STELZER, JULIAN · 2021 to 2024
$2.5M
Biological Basis of Genetic cMyBP-C CardiomyopathiesR01HL173989 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI Kenneth S Campbell, Julian Stelzer · 2024 to 2026
$2.0M
Molecular Basis for cMyBP-C HCM variantsR01HL175803 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI KRISHNA CHINTHALAPUDI, Julian Stelzer · 2025 to 2026
$1.4M
American Heart Association-American Stroke Association 961478NHLBI NIH HHS R01 HL146676NHLBI NIH HHS R01 HL153236NHLBI NIH HHS R01 HL173989NHLBI NIH HHS R01 HL175803NIH HHS 1R01HL175803-01A1NIH HHS 5R01HL153236-04NIH HHS 5R01HL173989-02
6 · The paper itself

Abstract

Left ventricular hypertrophy (LVH) refers to the pathological thickening of the myocardial wall and is strongly associated with several adverse cardiac outcomes and sudden cardiac death. While the biomechanical drivers of LVH are well established, growing evidence points to a critical role for cardiac and systemic metabolism in modulating hypertrophic remodeling and disease pathogenesis. Despite the efficiency of fatty acid oxidation (FAO), LVH hearts preferentially increase glucose uptake and catabolism to drive glycolysis and oxidative phosphorylation (OXPHOS). The development of therapies to increase and enhance LFCA FAO is underway, with promising results. However, the mechanisms of systemic metabolic states and LCFA dynamics in the context of cardiac hypertrophy remain incompletely understood. Further, it is unknown to what extent cardiac metabolism is influenced by whole-body energy balance and lipid profiles, despite the common occurrence of lipotoxicity in LVH. In this study, we measured whole-body and cellular respiration along with analysis of lipid and glycogen stores in a mouse model of LVH. We found that loss of the cardiac-specific gene,

Indexed as

Hypertrophy, Left VentricularAnimalsDisease Models, AnimalEnergy MetabolismFatty AcidsLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaMuscle, SkeletalMyocardiumOxidative PhosphorylationFatty Acidscardiac lipotoxicitycardiac myosin-binding protein Cleft ventricular hypertrophylong-chain fatty acidsystemic metabolism

Identifiers

PMID41155405
PMCPMC12562477

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.