J
James L. Zellner
Researcher at Medical University of South Carolina
Publications - 42
Citations - 2485
James L. Zellner is an academic researcher from Medical University of South Carolina. The author has contributed to research in topics: Endothelin receptor & Heart failure. The author has an hindex of 22, co-authored 42 publications receiving 2433 citations.
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Journal ArticleDOI
A Matrix Metalloproteinase Induction/Activation System Exists in the Human Left Ventricular Myocardium and Is Upregulated in Heart Failure
Francis G. Spinale,Mytsi L. Coker,Lena J. Heung,Brian R. Bond,Himali R. Gunasinghe,Takuma Etoh,Aron T. Goldberg,James L. Zellner,A. Jackson Crumbley +8 more
TL;DR: Increased LV myocardial MMP activity and selective upregulation of MMPs with nonischemic and ischemic forms of DCM occurred and a local MMP induction/activation system was identified in isolated normal human LV myocytes that was upregulated with DCM.
Journal ArticleDOI
Increased matrix metalloproteinase activity and selective upregulation in LV myocardium from patients with end-stage dilated cardiomyopathy.
Chadwick V. Thomas,Mytsi L. Coker,James L. Zellner,John R. Handy,A. Jackson Crumbley,Francis G. Spinale +5 more
TL;DR: Increased LV myocardial MMP activity and evidence for independent regulatory mechanisms of MMP and TIMP expression with DCM suggest that selective inhibition of M MP species within the LVMyocardium may provide a novel therapeutic target in patients withDCM.
Journal ArticleDOI
Myocardial matrix degradation and metalloproteinase activation in the failing heart: a potential therapeutic target
TL;DR: Increased LV myocardial MMP expression and activity are contributory factors in the LV remodeling process in cardiomyopathic disease states and Regulation of myocardian MMPexpression and activity may be an important therapeutic target for controlling myocardia matrix remodeling in the setting of developing heart failure.
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Collagen remodeling and changes in LV function during development and recovery from supraventricular tachycardia.
Francis G. Spinale,Masaaki Tomita,James L. Zellner,J. C. Cook,Fred A. Crawford,Michael R. Zile +5 more
TL;DR: Early recovery from SVT was associated with LV hypertrophy, increased collagen, and increased LV stiffness, and chronic SVT resulted in systolic and diastolic dysfunction and reduced collagen support of adjoining myocytes.
Journal ArticleDOI
Relation between ventricular and myocyte remodeling with the development and regression of supraventricular tachycardia-induced cardiomyopathy.
TL;DR: In the PST group, LV fractional shortening returned to control values; however, there was persistent dilatation (end-diastolic dimension: 4.2 +/- 0.1 cm, p less than 0.05), and LV hypertrophy developed (3.3 +/-0.8 versus 3.7 versus 54.7 +/- 1.2 cm), which was observed in the control group.