FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy.
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Robert J. Vincent | L. Bonewald | M. Wacker | Jason R. Stubbs | C. Touchberry | B. Dawn | Lori A Wetmore | M. Girgis | Troy M Green | Vladimir Tchikrizov | J. Mannix | Tiffany F Mao | Brandon W Carney
[1] L. Bonewald,et al. FGF23 production by osteocytes , 2013, Pediatric Nephrology.
[2] J. Ketelslegers,et al. C-terminal FGF23 is a strong predictor of survival in systolic heart failure , 2012, Peptides.
[3] T. Basturk,et al. Relationship of Fibroblast Growth Factor 23 with Left Ventricle Mass Index and Coronary Calcificaton in Chronic Renal Disease , 2012, Kidney and Blood Pressure Research.
[4] B. Kestenbaum,et al. Fibroblast Growth Factor-23 and Death, Heart Failure, and Cardiovascular Events in Community-living Individuals Chs (cardiovascular Health Study) , 2022 .
[5] W. Richards,et al. FGF23 neutralization improves chronic kidney disease-associated hyperparathyroidism yet increases mortality. , 2012, The Journal of clinical investigation.
[6] T. Szekeres,et al. Inorganic phosphate and FGF‐23 predict outcome in stable systolic heart failure , 2012, European journal of clinical investigation.
[7] L. Tomlinson,et al. FGF-23 and osteoprotegerin are independently associated with myocardial damage in chronic kidney disease stages 3 and 4. Another link between chronic kidney disease-mineral bone disorder and the heart. , 2012, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[8] J. Molkentin,et al. Unraveling the secrets of a double life: contractile versus signaling Ca2+ in a cardiac myocyte. , 2012, Journal of molecular and cellular cardiology.
[9] Jason R. Stubbs,et al. Longitudinal evaluation of FGF23 changes and mineral metabolism abnormalities in a mouse model of chronic kidney disease , 2012, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[10] S. Booth,et al. FGF‐23 is associated with cardiac troponin T and mortality in hemodialysis patients , 2011, Hemodialysis international. International Symposium on Home Hemodialysis.
[11] M. Wacker,et al. Store-operated calcium entry is present in HL-1 cardiomyocytes and contributes to resting calcium. , 2011, Biochemical and biophysical research communications.
[12] A. Go,et al. FGF23 induces left ventricular hypertrophy. , 2011, The Journal of clinical investigation.
[13] D. Fliser,et al. The phosphatonin fibroblast growth factor 23 links calcium-phosphate metabolism with left-ventricular dysfunction and atrial fibrillation. , 2011, European heart journal.
[14] L. Ferrucci,et al. Relationship of serum fibroblast growth factor 23 with cardiovascular disease in older community-dwelling women. , 2011, European journal of endocrinology.
[15] E. Rimm,et al. Plasma fibroblast growth factor 23, parathyroid hormone, phosphorus, and risk of coronary heart disease. , 2011, American heart journal.
[16] L. Quarles,et al. Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype. , 2011, American journal of physiology. Endocrinology and metabolism.
[17] R. Girgert,et al. Renal protective effects of aliskiren beyond its antihypertensive property in a mouse model of progressive fibrosis. , 2011, American journal of hypertension.
[18] M. Ackerman,et al. Junctophilin-2 Expression Silencing Causes Cardiocyte Hypertrophy and Abnormal Intracellular Calcium-Handling , 2011, Circulation. Heart failure.
[19] J. Molkentin,et al. TRPC Channels As Effectors of Cardiac Hypertrophy , 2011, Circulation research.
[20] Robert J. Vincent,et al. Transplantation of expanded bone marrow-derived very small embryonic-like stem cells (VSEL-SCs) improves left ventricular function and remodelling after myocardial infarction , 2010, Journal of cellular and molecular medicine.
[21] 根岸 一明. Association between fibroblast growth factor 23 and left ventricular hypertrophy in maintenance hemodialysis patients : comparison with B-type natriuretic peptide and cardiac troponin T , 2011 .
[22] K. Ozono,et al. Both FGF23 and extracellular phosphate activate Raf/MEK/ERK pathway via FGF receptors in HEK293 cells , 2010, Journal of cellular biochemistry.
[23] M. Wacker,et al. Phosphatidylinositol 3,5-Bisphosphate (PI(3,5)P2) Potentiates Cardiac Contractility via Activation of the Ryanodine Receptor* , 2010, The Journal of Biological Chemistry.
[24] H. Jüppner,et al. Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. , 2010, Annual review of medicine.
[25] H. Melhus,et al. Serum intact FGF23 associate with left ventricular mass, hypertrophy and geometry in an elderly population. , 2009, Atherosclerosis.
[26] R. Pereira,et al. Patterns of FGF-23, DMP1, and MEPE expression in patients with chronic kidney disease. , 2009, Bone.
[27] J. Schmitt,et al. Cardiac hypertrophy: targeting Raf/MEK/ERK1/2-signaling. , 2009, The international journal of biochemistry & cell biology.
[28] M. Wacker,et al. Inhibition of Thromboxane A2-Induced Arrhythmias and Intracellular Calcium Changes in Cardiac Myocytes by Blockade of the Inositol Trisphosphate Pathway , 2009, Journal of Pharmacology and Experimental Therapeutics.
[29] L. Lind,et al. Relationship between circulating FGF23 and total body atherosclerosis in the community. , 2009, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[30] Thomas J. Wang,et al. Fibroblast Growth Factor 23 and Left Ventricular Hypertrophy in Chronic Kidney Disease , 2009, Circulation.
[31] K. Brunt,et al. Heme Oxygenase-1 Inhibits Pro-Oxidant Induced Hypertrophy in HL-1 Cardiomyocytes , 2009, Experimental biology and medicine.
[32] F. Kronenberg,et al. Pro-A-type natriuretic peptide and pro-adrenomedullin predict progression of chronic kidney disease: the MMKD Study. , 2009, Kidney international.
[33] Mai-Szu Wu,et al. Fibroblast Growth Factor 23: A Possible Cause of Left Ventricular Hypertrophy in Hemodialysis Patients , 2009, The American journal of the medical sciences.
[34] D. Michele,et al. Blebbistatin extends culture life of adult mouse cardiac myocytes and allows efficient and stable transgene expression. , 2008, American journal of physiology. Heart and circulatory physiology.
[35] D. Bers. Calcium cycling and signaling in cardiac myocytes. , 2008, Annual review of physiology.
[36] B. Ewald,et al. Meta‐analysis of B type natriuretic peptide and N‐terminal pro B natriuretic peptide in the diagnosis of clinical heart failure and population screening for left ventricular systolic dysfunction , 2008, Internal medicine journal.
[37] M. Mohammadi,et al. The parathyroid is a target organ for FGF23 in rats. , 2007, The Journal of clinical investigation.
[38] F. Kronenberg,et al. B-type natriuretic peptide concentrations predict the progression of nondiabetic chronic kidney disease: the Mild-to-Moderate Kidney Disease Study. , 2007, Clinical chemistry.
[39] M. Fishbein,et al. Hypertrophy and heart failure in mice overexpressing the cardiac sodium-calcium exchanger. , 2007, Journal of cardiac failure.
[40] K. Okawa,et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23 , 2006, Nature.
[41] L. Bonewald,et al. Loss of DMP1 causes rickets and osteomalacia and identifies a role for osteocytes in mineral metabolism , 2006, Nature Genetics.
[42] Shaun K Olsen,et al. Receptor Specificity of the Fibroblast Growth Factor Family , 2006, Journal of Biological Chemistry.
[43] M. Econs,et al. Sensitivity of fibroblast growth factor 23 measurements in tumor-induced osteomalacia. , 2006, The Journal of clinical endocrinology and metabolism.
[44] R. Bolli,et al. Postinfarct Cytokine Therapy Regenerates Cardiac Tissue and Improves Left Ventricular Function , 2006, Circulation research.
[45] K. White,et al. Analysis of the biochemical mechanisms for the endocrine actions of fibroblast growth factor-23. , 2005, Endocrinology.
[46] M. Wacker,et al. Analysis of one-step and two-step real-time RT-PCR using SuperScript III. , 2005, Journal of biomolecular techniques : JBT.
[47] B. Chandrasekar,et al. Interleukin-18 Is a Pro-hypertrophic Cytokine That Acts through a Phosphatidylinositol 3-Kinase-Phosphoinositide-dependent Kinase-1-Akt-GATA4 Signaling Pathway in Cardiomyocytes* , 2005, Journal of Biological Chemistry.
[48] W. Bloch,et al. Antifibrotic, nephroprotective potential of ACE inhibitor vs AT1 antagonist in a murine model of renal fibrosis. , 2004, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[49] M. Inaba,et al. FGF-23 in patients with end-stage renal disease on hemodialysis. , 2004, Kidney international.
[50] K. Kamiya,et al. Sinoatrial Node Dysfunction and Early Unexpected Death of Mice With a Defect of klotho Gene Expression , 2004, Circulation.
[51] H. Jüppner,et al. Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy volunteers. , 2003, Kidney international.
[52] R. Panek,et al. In vitro biological characterization and antiangiogenic effects of PD 166866, a selective inhibitor of the FGF-1 receptor tyrosine kinase. , 1998, The Journal of pharmacology and experimental therapeutics.
[53] N J Izzo,et al. HL-1 cells: a cardiac muscle cell line that contracts and retains phenotypic characteristics of the adult cardiomyocyte. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[54] Tadashi Kaname,et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing , 1997, Nature.
[55] S. Hughes,et al. Differential Expression of the Fibroblast Growth Factor Receptor (FGFR) Multigene Family in Normal Human Adult Tissues , 1997, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[56] J. Rozich,et al. Rapid expression of the Na(+)-Ca2+ exchanger in response to cardiac pressure overload. , 1993, The American journal of physiology.
[57] N. Reichek,et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. , 1989, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.
[58] A. DeMaria,et al. Recommendations Regarding Quantitation in M-Mode Echocardiography: Results of a Survey of Echocardiographic Measurements , 1978, Circulation.
[59] R Gorlin,et al. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy. , 1976, The American journal of cardiology.