A maladaptive feedback mechanism between the extracellular matrix and cytoskeleton contributes to hypertrophic cardiomyopathy pathophysiology

[1]  Yu Suk Choi,et al.  Interrogating cardiac muscle cell mechanobiology on stiffness gradient hydrogels. , 2021, Biomaterials science.

[2]  C. D. dos Remedios,et al.  Proteomic and Functional Studies Reveal Detyrosinated Tubulin as Treatment Target in Sarcomere Mutation-Induced Hypertrophic Cardiomyopathy , 2021, Circulation. Heart failure.

[3]  Victoria P. A. Johnstone,et al.  Characterization and validation of a preventative therapy for hypertrophic cardiomyopathy in a murine model of the disease , 2020, Proceedings of the National Academy of Sciences.

[4]  Yu Suk Choi,et al.  Stem Cell Mechanosensation on Gelatin Methacryloyl (GelMA) Stiffness Gradient Hydrogels , 2019, Annals of Biomedical Engineering.

[5]  Yu Suk Choi,et al.  Volume adaptation controls stem cell mechanotransduction. , 2019, ACS applied materials & interfaces.

[6]  Jinkyu Park,et al.  Extracellular Matrix From Hypertrophic Myocardium Provokes Impaired Twitch Dynamics in Healthy Cardiomyocytes , 2019, JACC. Basic to translational science.

[7]  L. Hool,et al.  Impaired calcium handling and mitochondrial metabolic dysfunction as early markers of hypertrophic cardiomyopathy. , 2019, Archives of biochemistry and biophysics.

[8]  M. Tanter,et al.  Myocardial Stiffness Evaluation Using Noninvasive Shear Wave Imaging in Healthy and Hypertrophic Cardiomyopathic Adults , 2019, JACC. Cardiovascular imaging.

[9]  J. Sadoshima,et al.  New Insights Into the Role of mTOR Signaling in the Cardiovascular System. , 2018, Circulation Research.

[10]  Cynthia A. Reinhart-King,et al.  Targeting extracellular matrix stiffness to attenuate disease: From molecular mechanisms to clinical trials , 2018, Science Translational Medicine.

[11]  M. Sabater-Molina,et al.  Genetics of hypertrophic cardiomyopathy: A review of current state , 2018, Clinical genetics.

[12]  E. Braunwald,et al.  Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy. , 2017, Circulation research.

[13]  Joachim P Spatz,et al.  Stem cell migration and mechanotransduction on linear stiffness gradient hydrogels , 2017, Proceedings of the National Academy of Sciences.

[14]  T. Minamino,et al.  Physiological and pathological cardiac hypertrophy. , 2016, Journal of molecular and cellular cardiology.

[15]  Victoria P. A. Johnstone,et al.  The L‐type Ca2+ channel facilitates abnormal metabolic activity in the cTnI‐G203S mouse model of hypertrophic cardiomyopathy , 2016, The Journal of physiology.

[16]  M. Brink,et al.  mTOR, cardiomyocytes and inflammation in cardiac hypertrophy. , 2016, Biochimica et biophysica acta.

[17]  Victoria P. A. Johnstone,et al.  The Role of the L-Type Ca2+ Channel in Altered Metabolic Activity in a Murine Model of Hypertrophic Cardiomyopathy , 2016, JACC. Basic to translational science.

[18]  S. Campbell,et al.  The Structural Basis of Actin Organization by Vinculin and Metavinculin. , 2016, Journal of molecular biology.

[19]  J. Omens,et al.  Mechanotransduction in cardiac hypertrophy and failure. , 2015, Circulation research.

[20]  J. Sanger,et al.  Jasplakinolide reduces actin and tropomyosin dynamics during myofibrillogenesis , 2014, Cytoskeleton.

[21]  L. Hool,et al.  Impaired functional communication between the L-type calcium channel and mitochondria contributes to metabolic inhibition in the mdx heart , 2014, Proceedings of the National Academy of Sciences.

[22]  R. Ross,et al.  Integrins and integrin-associated proteins in the cardiac myocyte. , 2014, Circulation research.

[23]  Yu Suk Choi,et al.  In situ mechanotransduction via vinculin regulates stem cell differentiation , 2013, Stem cells.

[24]  Dennis E. Discher,et al.  Nuclear Lamin-A Scales with Tissue Stiffness and Enhances Matrix-Directed Differentiation , 2013, Science.

[25]  Deepak L. Bhatt,et al.  2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. , 2013, Circulation.

[26]  Barry J Maron,et al.  2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. , 2011, The Journal of thoracic and cardiovascular surgery.

[27]  Kevin Kit Parker,et al.  Mechanotransduction: the role of mechanical stress, myocyte shape, and cytoskeletal architecture on cardiac function , 2011, Pflügers Archiv - European Journal of Physiology.

[28]  S. Colan,et al.  Myocardial fibrosis as an early manifestation of hypertrophic cardiomyopathy. , 2010, The New England journal of medicine.

[29]  Adam J Engler,et al.  Preparation of Hydrogel Substrates with Tunable Mechanical Properties , 2010, Current protocols in cell biology.

[30]  L. Hool,et al.  Cross‐talk between L‐type Ca2+ channels and mitochondria , 2010, Clinical and experimental pharmacology & physiology.

[31]  B. Maron.  Contemporary Reviews in Cardiovascular Medicine Contemporary Insights and Strategies for Risk Stratification and Prevention of Sudden Death in Hypertrophic Cardiomyopathy , 2010 .

[32]  P. Arthur,et al.  Evidence for regulation of mitochondrial function by the L-type Ca2+ channel in ventricular myocytes. , 2009, Journal of molecular and cellular cardiology.

[33]  G. Church,et al.  Polony Multiplex Analysis of Gene Expression (PMAGE) in Mouse Hypertrophic Cardiomyopathy , 2007, Science.

[34]  T. O’Connell,et al.  Isolation and culture of adult mouse cardiac myocytes. , 2007, Methods in molecular biology.

[35]  J. Coles,et al.  Integrin-Linked Kinase Expression Is Elevated in Human Cardiac Hypertrophy and Induces Hypertrophy in Transgenic Mice , 2006, Circulation.

[36]  D. Allen,et al.  Molecular insights from a novel cardiac troponin I mouse model of familial hypertrophic cardiomyopathy. , 2006, Journal of molecular and cellular cardiology.

[37]  Emilio Hirsch,et al.  Integrin signalling: the tug-of-war in heart hypertrophy. , 2006, Cardiovascular research.

[38]  ElizabethMurphy,et al.  Mitochondrial Dysfunction and Apoptosis Underlie the Pathogenic Process in α-B-Crystallin Desmin-Related Cardiomyopathy , 2005 .

[39]  P. Oliviéro,et al.  Cytoskeleton and mitochondrial morphology and function , 1998, Molecular and Cellular Biochemistry.

[40]  A. Blamire,et al.  Hypertrophic cardiomyopathy due to sarcomeric gene mutations is characterized by impaired energy metabolism irrespective of the degree of hypertrophy. , 2003, Journal of the American College of Cardiology.

[41]  Y. Capetanaki.  Desmin cytoskeleton: a potential regulator of muscle mitochondrial behavior and function. , 2002, Trends in cardiovascular medicine.

[42]  R. Balaban.  Cardiac energy metabolism homeostasis: role of cytosolic calcium. , 2002, Journal of molecular and cellular cardiology.

[43]  J. Behlke,et al.  The carboxyl‐terminal region of ahnak provides a link between cardiac L‐type Ca2+ channels and the actinbased cytoskeleton , 2002, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[44]  D. Bers.  Cardiac excitation–contraction coupling , 2002, Nature.

[45]  R. Ross,et al.  Integrins and the myocardium. , 2001, Genetic engineering.

[46]  A. Marian,et al.  The molecular genetic basis for hypertrophic cardiomyopathy. , 2001, Journal of molecular and cellular cardiology.

[47]  N. Klugbauer,et al.  Modulation of the smooth-muscle L-type Ca2+ channel alpha1 subunit (alpha1C-b) by the beta2a subunit: a peptide which inhibits binding of beta to the I-II linker of alpha1 induces functional uncoupling. , 2000, The Biochemical journal.

[48]  V. Mootha,et al.  Ca2+ activation of heart mitochondrial oxidative phosphorylation: role of the F0/F1-ATPase , 2000 .

[49]  G. Vassort,et al.  Microtubule disruption modulates Ca(2+) signaling in rat cardiac myocytes. , 2000, Circulation research.

[50]  V. Mootha,et al.  Ca(2+) activation of heart mitochondrial oxidative phosphorylation: role of the F(0)/F(1)-ATPase. , 2000, American journal of physiology. Cell physiology.

[51]  K. Campbell,et al.  Calcium channel β-subunit binds to a conserved motif in the I–II cytoplasmic linker of the α1-subunit , 1994, Nature.