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Computational model of cardiomyocyte apoptosis identifies mechanisms of tyrosine kinase inhibitor-induced cardiotoxicity.

Journal of molecular and cellular cardiology

Grabowska ME, Chun B, Moya R, Saucerman JJ.
PMID: 33667419
J Mol Cell Cardiol. 2021 Jun;155:66-77. doi: 10.1016/j.yjmcc.2021.02.014. Epub 2021 Mar 03.

Despite clinical observations of cardiotoxicity among cancer patients treated with tyrosine kinase inhibitors (TKIs), the molecular mechanisms by which these drugs affect the heart remain largely unknown. Mechanistic understanding of TKI-induced cardiotoxicity has been limited in part due to...

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Grabowska ME, Chun B, Moya R, et al. Computational model of cardiomyocyte apoptosis identifies mechanisms of tyrosine kinase inhibitor-induced cardiotoxicity. J Mol Cell Cardiol. 2021;155:66-77doi: 10.1016/j.yjmcc.2021.02.014.
Grabowska, M. E., Chun, B., Moya, R., & Saucerman, J. J. (2021). Computational model of cardiomyocyte apoptosis identifies mechanisms of tyrosine kinase inhibitor-induced cardiotoxicity. Journal of molecular and cellular cardiology, 15566-77. https://doi.org/10.1016/j.yjmcc.2021.02.014
Grabowska, Monika E, et al. "Computational model of cardiomyocyte apoptosis identifies mechanisms of tyrosine kinase inhibitor-induced cardiotoxicity." Journal of molecular and cellular cardiology vol. 155 (2021): 66-77. doi: https://doi.org/10.1016/j.yjmcc.2021.02.014
Grabowska ME, Chun B, Moya R, Saucerman JJ. Computational model of cardiomyocyte apoptosis identifies mechanisms of tyrosine kinase inhibitor-induced cardiotoxicity. J Mol Cell Cardiol. 2021 Jun;155:66-77. doi: 10.1016/j.yjmcc.2021.02.014. Epub 2021 Mar 03. PMID: 33667419; PMCID: PMC8154673.
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Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies.

Current opinion in biomedical engineering

Aboelkassem Y, Powers JD, McCabe KJ, McCulloch AD.
PMID: 31886450
Curr Opin Biomed Eng. 2019 Sep;11:35-44. doi: 10.1016/j.cobme.2019.09.005. Epub 2019 Sep 18.

Myocardial hypertrophy is the result of sustained perturbations to the mechanical and/or neurohormonal homeostasis of cardiac cells and is driven by integrated, multiscale biophysical and biochemical processes that are currently not well defined. In this brief review, we highlight...

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Aboelkassem Y, Powers JD, McCabe KJ, et al. Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies. Curr Opin Biomed Eng. 2019;11:35-44doi: 10.1016/j.cobme.2019.09.005.
Aboelkassem, Y., Powers, J. D., McCabe, K. J., & McCulloch, A. D. (2019). Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies. Current opinion in biomedical engineering, 1135-44. https://doi.org/10.1016/j.cobme.2019.09.005
Aboelkassem, Yasser, et al. "Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies." Current opinion in biomedical engineering vol. 11 (2019): 35-44. doi: https://doi.org/10.1016/j.cobme.2019.09.005
Aboelkassem Y, Powers JD, McCabe KJ, McCulloch AD. Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies. Curr Opin Biomed Eng. 2019 Sep;11:35-44. doi: 10.1016/j.cobme.2019.09.005. Epub 2019 Sep 18. PMID: 31886450; PMCID: PMC6934086.
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Vinculin at the heart of aging.

Annals of translational medicine

Bradford WH, Omens JH, Sheikh F.
PMID: 28251141
Ann Transl Med. 2017 Feb;5(3):62. doi: 10.21037/atm.2017.01.65.

No abstract available.

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Bradford WH, Omens JH, Sheikh F. Vinculin at the heart of aging. Ann Transl Med. 2017;5(3):62doi: 10.21037/atm.2017.01.65.
Bradford, W. H., Omens, J. H., & Sheikh, F. (2017). Vinculin at the heart of aging. Annals of translational medicine, 5(3), 62. https://doi.org/10.21037/atm.2017.01.65
Bradford, William H, et al. "Vinculin at the heart of aging." Annals of translational medicine vol. 5,3 (2017): 62. doi: https://doi.org/10.21037/atm.2017.01.65
Bradford WH, Omens JH, Sheikh F. Vinculin at the heart of aging. Ann Transl Med. 2017 Feb;5(3):62. doi: 10.21037/atm.2017.01.65. PMID: 28251141; PMCID: PMC5326649.
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Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape.

Frontiers in pediatrics

Dewan S, Krishnamurthy A, Kole D, Conca G, Kerckhoffs R, Puchalski MD, Omens JH, Sun H, Nigam V, McCulloch AD.
PMID: 28275592
Front Pediatr. 2017 Feb 22;5:25. doi: 10.3389/fped.2017.00025. eCollection 2017.

INTRODUCTION: Hypoplastic left heart syndrome (HLHS) is a congenital condition with an underdeveloped left ventricle (LV) that provides inadequate systemic blood flow postnatally. The development of HLHS is postulated to be due to altered biomechanical stimuli during gestation. Predicting...

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Dewan S, Krishnamurthy A, Kole D, et al. Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape. Front Pediatr. 2017;5:25doi: 10.3389/fped.2017.00025.
Dewan, S., Krishnamurthy, A., Kole, D., Conca, G., Kerckhoffs, R., Puchalski, M. D., Omens, J. H., Sun, H., Nigam, V., & McCulloch, A. D. (2017). Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape. Frontiers in pediatrics, 525. https://doi.org/10.3389/fped.2017.00025
Dewan, Sukriti, et al. "Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape." Frontiers in pediatrics vol. 5 (2017): 25. doi: https://doi.org/10.3389/fped.2017.00025
Dewan S, Krishnamurthy A, Kole D, Conca G, Kerckhoffs R, Puchalski MD, Omens JH, Sun H, Nigam V, McCulloch AD. Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape. Front Pediatr. 2017 Feb 22;5:25. doi: 10.3389/fped.2017.00025. eCollection 2017. PMID: 28275592; PMCID: PMC5319967.
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Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype.

Frontiers in physiology

Dewan S, McCabe KJ, Regnier M, McCulloch AD.
PMID: 28352236
Front Physiol. 2017 Mar 14;8:151. doi: 10.3389/fphys.2017.00151. eCollection 2017.

Dilated Cardiomyopathy (DCM) is a leading cause of sudden cardiac death characterized by impaired pump function and dilatation of cardiac ventricles. In this review we discuss various

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Dewan S, McCabe KJ, Regnier M, et al. Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype. Front Physiol. 2017;8:151doi: 10.3389/fphys.2017.00151.
Dewan, S., McCabe, K. J., Regnier, M., & McCulloch, A. D. (2017). Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype. Frontiers in physiology, 8151. https://doi.org/10.3389/fphys.2017.00151
Dewan, Sukriti, et al. "Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype." Frontiers in physiology vol. 8 (2017): 151. doi: https://doi.org/10.3389/fphys.2017.00151
Dewan S, McCabe KJ, Regnier M, McCulloch AD. Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype. Front Physiol. 2017 Mar 14;8:151. doi: 10.3389/fphys.2017.00151. eCollection 2017. PMID: 28352236; PMCID: PMC5348544.
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Mechano-Electric Coupling and Arrhythmogenic Current Generation in a Computational Model of Coupled Myocytes.

Frontiers in physiology

Timmermann V, McCulloch AD.
PMID: 33362569
Front Physiol. 2020 Dec 10;11:519951. doi: 10.3389/fphys.2020.519951. eCollection 2020.

A wide range of arrhythmogenic phenotypes have been associated with heterogeneous mechanical dyskinesis. Pro-arrhythmic effects are often associated with dysregulated intra-cellular calcium handling, especially

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Timmermann V, McCulloch AD. Mechano-Electric Coupling and Arrhythmogenic Current Generation in a Computational Model of Coupled Myocytes. Front Physiol. 2020;11:519951doi: 10.3389/fphys.2020.519951.
Timmermann, V., & McCulloch, A. D. (2020). Mechano-Electric Coupling and Arrhythmogenic Current Generation in a Computational Model of Coupled Myocytes. Frontiers in physiology, 11519951. https://doi.org/10.3389/fphys.2020.519951
Timmermann, Viviane, and McCulloch, Andrew D. "Mechano-Electric Coupling and Arrhythmogenic Current Generation in a Computational Model of Coupled Myocytes." Frontiers in physiology vol. 11 (2020): 519951. doi: https://doi.org/10.3389/fphys.2020.519951
Timmermann V, McCulloch AD. Mechano-Electric Coupling and Arrhythmogenic Current Generation in a Computational Model of Coupled Myocytes. Front Physiol. 2020 Dec 10;11:519951. doi: 10.3389/fphys.2020.519951. eCollection 2020. PMID: 33362569; PMCID: PMC7758443.
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Network model-based screen for FDA-approved drugs affecting cardiac fibrosis.

CPT: pharmacometrics & systems pharmacology

Zeigler AC, Chandrabhatla AS, Christiansen SL, Nelson AR, Holmes JW, Saucerman JJ.
PMID: 33571402
CPT Pharmacometrics Syst Pharmacol. 2021 Apr;10(4):377-388. doi: 10.1002/psp4.12599. Epub 2021 Feb 27.

Cardiac fibrosis is a significant component of pathological heart remodeling, yet it is not directly targeted by existing drugs. Systems pharmacology approaches have the potential to provide mechanistic frameworks with which to predict and understand how drugs modulate biological...

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Zeigler AC, Chandrabhatla AS, Christiansen SL, et al. Network model-based screen for FDA-approved drugs affecting cardiac fibrosis. CPT Pharmacometrics Syst Pharmacol. 2021;10(4):377-388doi: 10.1002/psp4.12599.
Zeigler, A. C., Chandrabhatla, A. S., Christiansen, S. L., Nelson, A. R., Holmes, J. W., & Saucerman, J. J. (2021). Network model-based screen for FDA-approved drugs affecting cardiac fibrosis. CPT: pharmacometrics & systems pharmacology, 10(4), 377-388. https://doi.org/10.1002/psp4.12599
Zeigler, Angela C, et al. "Network model-based screen for FDA-approved drugs affecting cardiac fibrosis." CPT: pharmacometrics & systems pharmacology vol. 10,4 (2021): 377-388. doi: https://doi.org/10.1002/psp4.12599
Zeigler AC, Chandrabhatla AS, Christiansen SL, Nelson AR, Holmes JW, Saucerman JJ. Network model-based screen for FDA-approved drugs affecting cardiac fibrosis. CPT Pharmacometrics Syst Pharmacol. 2021 Apr;10(4):377-388. doi: 10.1002/psp4.12599. Epub 2021 Feb 27. PMID: 33571402; PMCID: PMC8099443.
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Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts.

Frontiers in physiology

Lewalle A, Land S, Carruth E, Frank LR, Lamata P, Omens JH, McCulloch AD, Niederer SA, Smith NP.
PMID: 29527171
Front Physiol. 2018 Feb 23;9:37. doi: 10.3389/fphys.2018.00037. eCollection 2018.

The cardiac system compensates for variations in physiological and pathophysiological conditions through a dynamic remodeling at the organ, tissue, and intracellular levels in order to maintain function. However, on longer time scales following the onset of ventricular pressure overload,...

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Lewalle A, Land S, Carruth E, et al. Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts. Front Physiol. 2018;9:37doi: 10.3389/fphys.2018.00037.
Lewalle, A., Land, S., Carruth, E., Frank, L. R., Lamata, P., Omens, J. H., McCulloch, A. D., Niederer, S. A., & Smith, N. P. (2018). Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts. Frontiers in physiology, 937. https://doi.org/10.3389/fphys.2018.00037
Lewalle, Alexandre, et al. "Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts." Frontiers in physiology vol. 9 (2018): 37. doi: https://doi.org/10.3389/fphys.2018.00037
Lewalle A, Land S, Carruth E, Frank LR, Lamata P, Omens JH, McCulloch AD, Niederer SA, Smith NP. Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts. Front Physiol. 2018 Feb 23;9:37. doi: 10.3389/fphys.2018.00037. eCollection 2018. PMID: 29527171; PMCID: PMC5829063.
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The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart.

Journal of clinical medicine

Herum KM, Lunde IG, McCulloch AD, Christensen G.
PMID: 28534817
J Clin Med. 2017 May 19;6(5). doi: 10.3390/jcm6050053.

Cardiac fibrosis, the excessive accumulation of extracellular matrix (ECM), remains an unresolved problem in most forms of heart disease. In order to be successful in preventing, attenuating or reversing cardiac fibrosis, it is essential to understand the processes leading...

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Herum KM, Lunde IG, McCulloch AD, et al. The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart. J Clin Med. 2017;6(5)doi: 10.3390/jcm6050053.
Herum, K. M., Lunde, I. G., McCulloch, A. D., & Christensen, G. (2017). The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart. Journal of clinical medicine, 6(5), . https://doi.org/10.3390/jcm6050053
Herum, Kate M, et al. "The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart." Journal of clinical medicine vol. 6,5 (2017). doi: https://doi.org/10.3390/jcm6050053
Herum KM, Lunde IG, McCulloch AD, Christensen G. The Soft- and Hard-Heartedness of Cardiac Fibroblasts: Mechanotransduction Signaling Pathways in Fibrosis of the Heart. J Clin Med. 2017 May 19;6(5). doi: 10.3390/jcm6050053. PMID: 28534817; PMCID: PMC5447944.
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Cardiac cell type-specific gene regulatory programs and disease risk association.

Science advances

Hocker JD, Poirion OB, Zhu F, Buchanan J, Zhang K, Chiou J, Wang TM, Zhang Q, Hou X, Li YE, Zhang Y, Farah EN, Wang A, McCulloch AD, Gaulton KJ, Ren B, Chi NC, Preissl S.
PMID: 33990324
Sci Adv. 2021 May 14;7(20). doi: 10.1126/sciadv.abf1444. Print 2021 May.

Misregulated gene expression in human hearts can result in cardiovascular diseases that are leading causes of mortality worldwide. However, the limited information on the genomic location of candidate cis-regulatory elements (cCREs) such as enhancers and promoters in distinct cardiac...

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Hocker JD, Poirion OB, Zhu F, et al. Cardiac cell type-specific gene regulatory programs and disease risk association. Sci Adv. 2021;7(20)doi: 10.1126/sciadv.abf1444.
Hocker, J. D., Poirion, O. B., Zhu, F., Buchanan, J., Zhang, K., Chiou, J., Wang, T. M., Zhang, Q., Hou, X., Li, Y. E., Zhang, Y., Farah, E. N., Wang, A., McCulloch, A. D., Gaulton, K. J., Ren, B., Chi, N. C., & Preissl, S. (2021). Cardiac cell type-specific gene regulatory programs and disease risk association. Science advances, 7(20), . https://doi.org/10.1126/sciadv.abf1444
Hocker, James D, et al. "Cardiac cell type-specific gene regulatory programs and disease risk association." Science advances vol. 7,20 (2021). doi: https://doi.org/10.1126/sciadv.abf1444
Hocker JD, Poirion OB, Zhu F, Buchanan J, Zhang K, Chiou J, Wang TM, Zhang Q, Hou X, Li YE, Zhang Y, Farah EN, Wang A, McCulloch AD, Gaulton KJ, Ren B, Chi NC, Preissl S. Cardiac cell type-specific gene regulatory programs and disease risk association. Sci Adv. 2021 May 14;7(20). doi: 10.1126/sciadv.abf1444. Print 2021 May. PMID: 33990324; PMCID: PMC8121433.
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Showing 1 to 10 of 10 entries