In one paragraphArticle in Science signaling, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
14 authors.
Yan SunDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.ORCID 0000-0002-8776-0832 Abhishek Kumar MishraDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.
Vasanth ChanrasekharDivision of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Michaela DoorDepartment of Cell and Molecular Physiology, Loyola University Chicago Stritch School of Medicine, Maywood, IL 60153, USA.ORCID 0009-0009-3131-2887 Chase W KessingerDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.ORCID 0000-0003-2711-0069 Bing XuDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.
Peiyang TangDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.
Yunan GaoDepartment of Cardiology, Fourth Affiliated Hospital of Harbin Medical University, 37 Yiyuan Street, Harbin, Heilongjiang 150001, China.ORCID 0000-0002-4381-4712 Sarah Kamli-SalinoUniversity of Aberdeen, School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, Aberdeen AB24 3FX, UK.ORCID 0000-0002-5107-5366 Katherine NelsonDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.ORCID 0009-0002-3131-2616 Mirela DelibegovicUniversity of Aberdeen, School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, Aberdeen AB24 3FX, UK.ORCID 0000-0001-6193-3152 E Dale AbelFraternal Order of Eagles Diabetes Research Center and Department of Medicine, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0001-5290-0738 Jonathan A KirkDepartment of Cell and Molecular Physiology, Loyola University Chicago Stritch School of Medicine, Maywood, IL 60153, USA.ORCID 0000-0002-5192-2860 Maria I KontaridisDepartment of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, NY 13501, USA.ORCID 0000-0002-6121-0533 Funding
The Role of RhoA in the Molecular Pathogenesis of Heart DiseaseR01HL102368 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI KONTARIDIS, MARIA I · 2010 to 2021
$5.1MGSK-3β Localizes to the Myofilament and Modifies its Function in Ischemic CardiomyopathyR01HL136737 · NHLBI · UNIVERSITY OF CHICAGO · PI JONATHAN A KIRK · 2017 to 2026
$4.5MTargeted inhibition of fibrosis for the prevention of heart failureR01HL122238 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MCCARTHY, JASON R. · 2015 to 2019
$4.0MNHLBI NIH HHS R01 HL102368NHLBI NIH HHS R01 HL122238NHLBI NIH HHS R01 HL136737
6 · The paper itselfAbstract
Cardiomyocytes (CMs) normally use fatty acid oxidation (FAO) as their primary energy source. In response to pathological stress, the substrate preference of CMs switches from FAO to glucose metabolism, leading to the development of heart failure. Obesity increases this pathological risk of cardiovascular disease. We focused on protein tyrosine phosphatase 1B (PTP1B), an inhibitor of insulin signaling, the abundance and activity of which are increased in brain, muscle, and adipose tissues in obese and/or diabetic animals and in obese human patients. We generated mice with CM-specific deficiency in PTP1B (
Indexed as
CardiomyopathiesDiet, High-FatMyocytes, CardiacProtein Tyrosine Phosphatase, Non-Receptor Type 1Signal TransductionAnimalsFatty AcidsGene DeletionGlucoseHumansMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumFatty AcidsGlucoseProtein Tyrosine Phosphatase, Non-Receptor Type 1Ptpn1 protein, mouse
Identifiers
PMID40694612
PMCPMC12445919
What OpenQuestion holds
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LicenceTDM
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