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Your search keyword '"Aronovitz, Mark"' showing total 15 results
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15 results on '"Aronovitz, Mark"'

3. Isolevuglandin-Modified Cardiac Proteins Drive CD4+ T-Cell Activation in the Heart and Promote Cardiac Dysfunction

Author

Ngwenyama, Njabulo, primary, Kirabo, Annet, additional, Aronovitz, Mark, additional, Velázquez, Francisco, additional, Carrillo-Salinas, Francisco, additional, Salvador, Ane M., additional, Nevers, Tania, additional, Amarnath, Venkataraman, additional, Tai, Albert, additional, Blanton, Robert M., additional, Harrison, David G., additional, and Alcaide, Pilar, additional

Published
2021
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9. Rapid Estrogen Receptor Signaling Is Essential for the Protective Effects of Estrogen Against Vascular Injury

Author

Bernelot Moens, Sophie J., primary, Schnitzler, Gavin R., additional, Nickerson, Moriah, additional, Guo, Huiming, additional, Ueda, Kazutaka, additional, Lu, Qing, additional, Aronovitz, Mark J., additional, Nickerson, Heather, additional, Baur, Wendy E., additional, Hansen, Ulla, additional, Iyer, Lakshmanan K., additional, and Karas, Richard H., additional

Published
2012
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10. Reduced Endoglin Activity Limits Cardiac Fibrosis and Improves Survival in Heart Failure

Author

Kapur, Navin K., primary, Wilson, Szuhuei, additional, Yunis, Adil A., additional, Qiao, Xiaoying, additional, Mackey, Emily, additional, Paruchuri, Vikram, additional, Baker, Corey, additional, Aronovitz, Mark J., additional, Karumanchi, S. Ananth, additional, Letarte, Michelle, additional, Kass, David A., additional, Mendelsohn, Michael E., additional, and Karas, Richard H., additional

Published
2012
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11. Abstract 5018: Soluble fms-like Tyrosine Kinase (sFLT1): A Biomarker of Endothelial Origin in Acute ST-segment Elevation Myocardial Infarction (STEMI)

Author

Kapur, Navin K, primary, Yunis, Adil A, additional, Nguyen, Tuan A, additional, Parpos, Peter, additional, Krishnamurthy, Barath, additional, Cross, Brian J, additional, Aronovitz, Mark, additional, Weintraub, Andrew, additional, Kimmelstiel, Carey, additional, Jaffe, Iris Z, additional, Karas, Richard H, additional, and Mendelsohn, Michael E, additional

Published
2009
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15. Abstract 14858: CRD-733, a Novel Phosphodiesterase 9 Inhibitor, Reverses Pressure Overload-Induced Cardiac Hypertrophy in Mice.

Author

Richards, Daniel A, Aronovitz, Mark J, Karas, Richard H, Bloomfield, Daniel M, Mendelsohn, Michael E, and Blanton, Robert M

Subjects
*CARDIAC hypertrophy, *CGMP-dependent protein kinase, *LEFT ventricular hypertrophy, *PHOSPHODIESTERASE inhibitors, *CYCLIC guanylic acid, *PROTEIN kinases
Abstract

Introduction: Myocardial cyclic GMP (cGMP) elevation and activation of cGMP-dependent protein kinase (PKG) have been shown to attenuate pathological cardiac hypertrophy and remodeling. Expression of cardiac phosphodiesterase 9A (PDE9) is increased in HF patients and in mouse models of cardiac hypertrophy. PDE9 catalyses the breakdown of cGMP and has been shown to promote cardiac hypertrophy. Recent evidence suggests that PDE9 inhibition may be beneficial in HF, increasing cGMP and exerting anti-hypertrophic effects via PKG stimulation. A novel PDE9 inhibitor, CRD-733, has demonstrated safety in both preclinical and human studies, but has not yet been studied in models of hypertrophy. Hypothesis: PDE9 inhibition with CRD-733 can reverse established pressure overload-induced LVH in a murine model of HF. Methods: Left ventricular hypertrophy (LVH) was induced by transaortic constriction (TAC) in male C57/BL6J mice (n=58), alongside sham controls (n=10). On day 7, after established LVH, TAC mice were randomized to vehicle (n=17); or to CRD-733 at doses of 200 (n=10), 600 (n=10), 1000 (n=10) or 2000 (n=11) mg/kg/day by oral gavage (days 7-21). Primary endpoints included organ weights, echocardiography and invasive hemodynamics. Results: TAC induced a 53% increase in LV weight normalized to tibia length in vehicle treated mice at day 21 (7.71±0.29mg/mm vs. sham 5.04±0.15mg/mm; P<0.001). This increase was attenuated in mice treated with 600, 1000, and 2000 mg/kg/day CRD-733 (maximum reduction of 2.0±0.11 mg/mm, to 5.71±0.26 mg/mm, 75% reduction from vehicle; P<0.001). These findings were associated with complete normalization of TAC-induced increases in lung mass (P<0.001) and trends towards lower LV end diastolic pressure in drug-treated TAC mice (13.0±1.4mmHg in CRD-733 600mg/kg/day vs. 21.0±3.1mmHg in vehicle; P=0.08). Echocardiographic analysis showed that TAC-induced cardiac hypertrophy and left atrial dilation were reversed from day 6 to day 20 with CRD-733 treatment, but not with vehicle (P<0.05). Conclusion: CRD-733 reversed TAC-induced cardiac hypertrophy in mice and led to a reduction in lung mass, left atrial size, and LV end diastolic pressure. These findings support the potential of CRD-733 as a novel therapeutic agent in HF. [ABSTRACT FROM AUTHOR]

Published
2018

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