Loss of ADAM15 Exacerbates Transition to Decompensated Myocardial Hypertrophy and Dilation Through Activation of the Calcineurin Pathway
暂无分享,去创建一个
C. Owen | J. Seubert | A. Viveiros | G. Oudit | Z. Kassiri | O. Julien | Preetinder K Aujla | Mei Hu | Tolga Kilic | Joshua Kranrod | Bridgette Hartley | Preetinder K. Aujla | Joshua W. Kranrod
[1] T. Abraham,et al. ADAM15 is required for optimal collagen cross-linking and scar formation following myocardial infarction. , 2022, Matrix biology : journal of the International Society for Matrix Biology.
[2] C. McCulloch,et al. Gelsolin is an important mediator of Angiotensin II‐induced activation of cardiac fibroblasts and fibrosis , 2021, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[3] N. Bildyug. Integrins in cardiac hypertrophy: lessons learned from culture systems , 2021, ESC heart failure.
[4] M. Friedberg,et al. Cardiac Fibrosis: Key Role of Integrins in Cardiac Homeostasis and Remodeling , 2021, Cells.
[5] C. Sergi,et al. The Human Explanted Heart Program: A translational bridge for cardiovascular medicine , 2020, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease.
[6] Catherine L. Worth,et al. Cells of the adult human heart , 2020, Nature.
[7] I. Shimomura,et al. A Disintegrin and Metalloproteinase 12 prevents heart failure by regulating cardiac hypertrophy and fibrosis. , 2019, American journal of physiology. Heart and circulatory physiology.
[8] Olga Tanaseichuk,et al. Metascape provides a biologist-oriented resource for the analysis of systems-level datasets , 2019, Nature Communications.
[9] J. Molkentin,et al. Thrombospondin-3 augments injury-induced cardiomyopathy by intracellular integrin inhibition and sarcolemmal instability , 2019, Nature Communications.
[10] H. Zhang,et al. Disparate Remodeling of the Extracellular Matrix and Proteoglycans in Failing Pediatric Versus Adult Hearts , 2018, Journal of the American Heart Association.
[11] J. Sadoshima,et al. Mechanisms of physiological and pathological cardiac hypertrophy , 2018, Nature Reviews Cardiology.
[12] Z. Kassiri,et al. Disintegrin and metalloproteinases (ADAMs and ADAM-TSs), the emerging family of proteases in heart physiology and pathology , 2018 .
[13] Youguo Ying,et al. The involvement of the laminin-integrin α7β1 signaling pathway in mechanical ventilation-induced pulmonary fibrosis. , 2017, Journal of thoracic disease.
[14] Xiuhua Wang,et al. Tissue Inhibitor of Matrix Metalloproteinase-1 Promotes Myocardial Fibrosis by Mediating CD63–Integrin &bgr;1 Interaction , 2017, Hypertension.
[15] Xiuhua Wang,et al. A Disintegrin and Metalloprotease-17 Regulates Pressure Overload–Induced Myocardial Hypertrophy and Dysfunction Through Proteolytic Processing of Integrin &bgr;1 , 2016, Hypertension.
[16] T. Minamino,et al. Physiological and pathological cardiac hypertrophy. , 2016, Journal of molecular and cellular cardiology.
[17] C. Sergi,et al. Differential impact of mechanical unloading on structural and nonstructural components of the extracellular matrix in advanced human heart failure. , 2016, Translational research : the journal of laboratory and clinical medicine.
[18] Z. Kassiri,et al. ADAMs family and relatives in cardiovascular physiology and pathology. , 2016, Journal of molecular and cellular cardiology.
[19] Xiuhua Wang,et al. Differential role of TIMP2 and TIMP3 in cardiac hypertrophy, fibrosis, and diastolic dysfunction. , 2014, Cardiovascular research.
[20] Xiuhua Wang,et al. Lack of tissue inhibitor of metalloproteinases 2 leads to exacerbated left ventricular dysfunction and adverse extracellular matrix remodeling in response to biomechanical stress. , 2011, Circulation.
[21] Yibin Wang,et al. Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. , 2010, Physiological reviews.
[22] M. Michalak,et al. Calreticulin: non‐endoplasmic reticulum functions in physiology and disease , 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[23] Cinzia Perrino,et al. Induction of Mitogen-Activated Protein Kinases Is Proportional to the Amount of Pressure Overload , 2010, Hypertension.
[24] X. Wehrens,et al. NFATc2 Is a Necessary Mediator of Calcineurin-dependent Cardiac Hypertrophy and Heart Failure* , 2008, Journal of Biological Chemistry.
[25] Xiaojing Ye,et al. The integrins , 2007, Genome Biology.
[26] M. Boppart,et al. Alpha7beta1-integrin regulates mechanotransduction and prevents skeletal muscle injury. , 2006, American journal of physiology. Cell physiology.
[27] J. Molkentin. Calcineurin-NFAT signaling regulates the cardiac hypertrophic response in coordination with the MAPKs. , 2004, Cardiovascular research.
[28] Jian Xu,et al. Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy , 2004, Circulation research.
[29] M. Michalak,et al. Calreticulin is an upstream regulator of calcineurin. , 2003, Biochemical and biophysical research communications.
[30] K. Horiuchi,et al. Potential Role for ADAM15 in Pathological Neovascularization in Mice , 2003, Molecular and Cellular Biology.
[31] R. Weiss,et al. Targeted Inhibition of Calcineurin in Pressure-overload Cardiac Hypertrophy , 2002, The Journal of Biological Chemistry.
[32] Laurence H. Pearl,et al. Crystal Structure of Glycogen Synthase Kinase 3β Structural Basis for Phosphate-Primed Substrate Specificity and Autoinhibition , 2001, Cell.
[33] C. Pham,et al. Striated muscle-specific beta(1D)-integrin and FAK are involved in cardiac myocyte hypertrophic response pathway. , 2000, American journal of physiology. Heart and circulatory physiology.
[34] S. Eom,et al. Calreticulin couples calcium release and calcium influx in integrin-mediated calcium signaling. , 2000, Molecular biology of the cell.
[35] D. Bouvard,et al. Calcium/calmodulin-dependent protein kinase II controls alpha5beta1 integrin-mediated inside-out signaling. , 1998, Journal of cell science.
[36] P. Frachet,et al. Control of the alpha 5 beta 1 integrin/fibronectin interaction in vitro by the serine/threonine protein phosphatase calcineurin. , 1995, Biochemistry.
[37] S. Dedhar,et al. Cell attachment to extracellular matrix substrates is inhibited upon downregulation of expression of calreticulin, an intracellular integrin alpha-subunit-binding protein. , 1994, Journal of cell science.