Cardiomyopathy in α-Kinase 3 (ALPK3)-Deficient Mice
Abstract
Cardiomyopathy developed in mice deficient for α-kinase 3 (ALPK3), a nuclear kinase previously implicated in the differentiation of cardiomyocytes. Alpk3 (-/-) mice were produced according to normal Mendelian ratios and appeared normal except for a nonprogressive cardiomyopathy that had features of both hypertrophic and dilated forms of cardiomyopathy. Cardiac hypertrophy in Alpk3 (-/-) mice was characterized by increased thickness of both left and right ventricular (LV and RV) walls and by markedly increased heart weight and increased heart weight/body weight and heart weight/tibia length ratios. Magnetic resonance imaging studies confirmed the increased thickness in both septal and LV free walls at end-diastole, although there was no significant change in LV wall thickness at end-systole. Myocardial hypertrophy was the predominant feature in Alpk3 (-/-) mice, but several changes more typically associated with dilated cardiomyopathy included a marked increase in end-diastolic and end-systolic LV volume, as well as reduced cardiac output, stroke volume, and ejection fractions, suggesting LV chamber dilation. Magnetic resonance imaging showed a 50% reduction in both septal and free wall LV contractility in Alpk3 (-/-) mice. Interstitial fibrosis and inflammation were notably absent in Alpk3 (-/-) mice; however, light and electron microscopy revealed altered cardiomyocyte architecture, characterized by reduced numbers of abnormal intercalated discs being associated with mild disarray of myofibrils. These lesions could account for the impaired contractility of the myofibrillar apparatus and contribute to the pathogenesis of cardiomyopathy in Alpk3 (-/-) mice.
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Knockout of ALPK3 in mice shows both hypertrophic and dilated forms of cardiomyopathy.
“ALPK3 encodes a kinase and plays a role in cardiomyocyte differentiation; knockout genes in mice show both hypertrophic and dilated forms of cardiomyopathy (Van Sligtenhorst et al., 2012).”
From Population genomics reveal recent speciation and rapid evolutionary adaptation in polar bears (2014) · cites this paper as Van Sligtenhorst et al., 2012
ALPK3 plays a role in cardiomyocyte differentiation.
“ALPK3 encodes a kinase and plays a role in cardiomyocyte differentiation; knockout genes in mice show both hypertrophic and dilated forms of cardiomyopathy (Van Sligtenhorst et al., 2012).”
From Population genomics reveal recent speciation and rapid evolutionary adaptation in polar bears (2014) · cites this paper as Van Sligtenhorst et al., 2012
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Wang, J., Wang, F., Wu, G., Lu, M., Zhang, C., Song, L., Shao, Y., Wang, J., Liu, F., & Zhang, M. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e32786 · Cited by 3 · see citing works
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Connecting intermediate phenotypes to disease using multi-omics in heart failurePreprint
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Identification and validation of hypoxia-responsive signature pathways in human cardiomyocytes
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Chang, C., Wang, L., Chen, Z., Bogomolovas, J., & Chen, J. (2025) · Circulation Genomic and Precision Medicine · doi:10.1161/circgen.125.005368
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- Authors
- Van Sligtenhorst, I., Ding, Z.-M., Shi, Z.-Z., Read, R. W., Hansen, G., & Vogel, P.
- Affiliations
- Department of Cardiology, Lexicon Pharmaceuticals Inc, The Woodlands, TX
- Lexicon Pharmaceuticals (United States) (US)
- Corresponding author
- Vogel, P.
- Venue
- Veterinary Pathology
- Publisher
- SAGE Publications
- Published
- 2011-03-25
- Volume
- 49
- Issue
- 1
- Pages
- 131-141
- ISSN
- 0300-9858 (ISSN-L)
- 1544-2217
- OpenAlex
- W2156080132
- Cited by
- 48
- References
- 43
- Citations by year
- 2025: 7 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 4 · 2020: 6 · 2019: 4 · 2018: 1 · 2017: 2 · 2016: 6 · 2015: 1 · 2014: 4
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Veterinary Pathology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- cardiomyopathy, ALPK3, nuclear kinase, cardiomyocyte differentiation, cardiac hypertrophy, dilated cardiomyopathy, left ventricular contractility, intercalated discs, myofibrillar disarray
- MeSH terms
- Animals, Diastole, Dobutamine, Female, Heart, Heart Failure, Heart Rate, Heart Ventricles, Humans, Male, Muscle Proteins, Myocardial Contraction, Cardiomyopathies, Myocardium, Phosphotransferases, Stroke Volume, Systole, Sequence Deletion, Mice, Knockout, Myocytes, Cardiac, Mice
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