"Heart" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
The hollow, muscular organ that maintains the circulation of the blood.
Descriptor ID |
D006321
|
MeSH Number(s) |
A07.541
|
Concept/Terms |
|
Below are MeSH descriptors whose meaning is more general than "Heart".
Below are MeSH descriptors whose meaning is more specific than "Heart".
This graph shows the total number of publications written about "Heart" by people in this website by year, and whether "Heart" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
Year | Major Topic | Minor Topic | Total |
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1995 | 1 | 0 | 1 |
1998 | 1 | 0 | 1 |
1999 | 1 | 0 | 1 |
2010 | 1 | 0 | 1 |
2011 | 0 | 1 | 1 |
2012 | 1 | 0 | 1 |
2015 | 1 | 0 | 1 |
2017 | 1 | 0 | 1 |
2019 | 1 | 0 | 1 |
2020 | 0 | 1 | 1 |
2021 | 1 | 0 | 1 |
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Below are the most recent publications written about "Heart" by people in Profiles.
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Creld1 regulates myocardial development and function. J Mol Cell Cardiol. 2021 07; 156:45-56.
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Cytosolic, but not matrix, calcium is essential for adjustment of mitochondrial pyruvate supply. J Biol Chem. 2020 04 03; 295(14):4383-4397.
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Mitochondrial Oxidative Phosphorylation defect in the Heart of Subjects with Coronary Artery Disease. Sci Rep. 2019 05 20; 9(1):7623.
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Adiponectin, biomarkers of inflammation and changes in cardiac autonomic function: Whitehall II study. Cardiovasc Diabetol. 2017 Dec 01; 16(1):153.
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Differential Patterns and Determinants of Cardiac Autonomic Nerve Dysfunction during Endotoxemia and Oral Fat Load in Humans. PLoS One. 2015; 10(4):e0124242.
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IGF-IR signaling attenuates the age-related decline of diastolic cardiac function. Am J Physiol Endocrinol Metab. 2012 Jul 15; 303(2):E213-22.
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MicroRNA profiling during cardiomyocyte-specific differentiation of murine embryonic stem cells based on two different miRNA array platforms. PLoS One. 2011; 6(10):e25809.
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Primary endothelial damage is the mechanism of cardiotoxicity of tubulin-binding drugs. Toxicol Sci. 2010 Sep; 117(1):144-51.
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Mouse model of a familial hypertrophic cardiomyopathy mutation in alpha-tropomyosin manifests cardiac dysfunction. Circ Res. 1999 Jul 09; 85(1):47-56.
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Beta-tropomyosin overexpression induces severe cardiac abnormalities. J Mol Cell Cardiol. 1998 Aug; 30(8):1545-57.