Zamaneh Kassiri

Summary

Affiliation: University of Alberta
Country: Canada

Publications

  1. doi request reprint Loss of PI3Kγ enhances cAMP-dependent MMP remodeling of the myocardial N-cadherin adhesion complexes and extracellular matrix in response to early biomechanical stress
    Danny Guo
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Canada
    Circ Res 107:1275-89. 2010
  2. pmc Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease
    Dong Fan
    Department of Physiology, University of Alberta, Edmonton, AB, T6G 2S2, Canada
    Fibrogenesis Tissue Repair 5:15. 2012
  3. pmc Loss of TIMP3 enhances interstitial nephritis and fibrosis
    Zamaneh Kassiri
    Department of Physiology, Cardiovascular Research Group, Room 474, Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, T6G 2S2 Canada
    J Am Soc Nephrol 20:1223-35. 2009
  4. doi request reprint Cardioprotective effects mediated by angiotensin II type 1 receptor blockade and enhancing angiotensin 1-7 in experimental heart failure in angiotensin-converting enzyme 2-null mice
    Vaibhav B Patel
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 59:1195-203. 2012
  5. pmc Enhanced susceptibility to biomechanical stress in ACE2 null mice is prevented by loss of the p47(phox) NADPH oxidase subunit
    Sreedhar Bodiga
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
    Cardiovasc Res 91:151-61. 2011
  6. pmc Early activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarction
    Vijay Kandalam
    Department of Physiology, University of Alberta, Edmonton, Alberta
    Am J Physiol Heart Circ Physiol 299:H1012-23. 2010
  7. doi request reprint Prevention of angiotensin II-mediated renal oxidative stress, inflammation, and fibrosis by angiotensin-converting enzyme 2
    Jiuchang Zhong
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 57:314-22. 2011
  8. doi request reprint Loss of p47phox subunit enhances susceptibility to biomechanical stress and heart failure because of dysregulation of cortactin and actin filaments
    Vaibhav B Patel
    Department of Medicine, Division of Cardiology, University of Alberta, Edmonton T6G 2S2, AB, Canada
    Circ Res 112:1542-56. 2013
  9. doi request reprint Angiotensin-converting enzyme 2 suppresses pathological hypertrophy, myocardial fibrosis, and cardiac dysfunction
    Jiuchang Zhong
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada
    Circulation 122:717-28, 18 p following 728. 2010
  10. doi request reprint Angiotensin-converting enzyme 2 is a critical determinant of angiotensin II-induced loss of vascular smooth muscle cells and adverse vascular remodeling
    Vaibhav B Patel
    From the Division of Cardiology, Department of Medicine V B P, n p, M S M, G Y O, Mazankowski Alberta Heart Institute V B P, D F, R B, n p, S T D, Z K, G Y O, Department of Physiology D F, R B, S T D, Z K, G Y O, and Department of Obstetrics and Gynecology J S M, S T D, University of Alberta, Edmonton, Alberta, Canada State Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China J C Z and Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Shanghai, China J C Z
    Hypertension 64:157-64. 2014

Collaborators

Detail Information

Publications45

  1. doi request reprint Loss of PI3Kγ enhances cAMP-dependent MMP remodeling of the myocardial N-cadherin adhesion complexes and extracellular matrix in response to early biomechanical stress
    Danny Guo
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Canada
    Circ Res 107:1275-89. 2010
    ..Loss of phosphoinositide 3-kinase (PI3K)γ, the isoform linked to G protein-coupled receptor signaling, results in increased myocardial contractility, but the response to pressure overload is controversial...
  2. pmc Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease
    Dong Fan
    Department of Physiology, University of Alberta, Edmonton, AB, T6G 2S2, Canada
    Fibrogenesis Tissue Repair 5:15. 2012
    ..We will further provide an overview of what we have learned from experimental animal models and genetically modified mice with altered expression of ECM regulatory proteins, MMPs and TIMPs...
  3. pmc Loss of TIMP3 enhances interstitial nephritis and fibrosis
    Zamaneh Kassiri
    Department of Physiology, Cardiovascular Research Group, Room 474, Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, T6G 2S2 Canada
    J Am Soc Nephrol 20:1223-35. 2009
    ..Taken together, these results provide evidence that TIMP3 is an important mediator of kidney injury, and regulating its activity may have therapeutic benefit for patients with kidney disease...
  4. doi request reprint Cardioprotective effects mediated by angiotensin II type 1 receptor blockade and enhancing angiotensin 1-7 in experimental heart failure in angiotensin-converting enzyme 2-null mice
    Vaibhav B Patel
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 59:1195-203. 2012
    ....
  5. pmc Enhanced susceptibility to biomechanical stress in ACE2 null mice is prevented by loss of the p47(phox) NADPH oxidase subunit
    Sreedhar Bodiga
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
    Cardiovasc Res 91:151-61. 2011
    ..Loss of ACE2 enhances the susceptibility to heart disease but the mechanism remains elusive. We hypothesized that ACE2 deficiency activates the NADPH oxidase system in pressure overload-induced heart failure...
  6. pmc Early activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarction
    Vijay Kandalam
    Department of Physiology, University of Alberta, Edmonton, Alberta
    Am J Physiol Heart Circ Physiol 299:H1012-23. 2010
    ..Hence, timing of treatments to improve cardiac response to MI may be critical in producing favorable outcome...
  7. doi request reprint Prevention of angiotensin II-mediated renal oxidative stress, inflammation, and fibrosis by angiotensin-converting enzyme 2
    Jiuchang Zhong
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 57:314-22. 2011
    ..ACE2 is an important negative regulator of Ang II-induced renal disease and enhancing ACE2 action may have therapeutic potential for patients with kidney disease...
  8. doi request reprint Loss of p47phox subunit enhances susceptibility to biomechanical stress and heart failure because of dysregulation of cortactin and actin filaments
    Vaibhav B Patel
    Department of Medicine, Division of Cardiology, University of Alberta, Edmonton T6G 2S2, AB, Canada
    Circ Res 112:1542-56. 2013
    ..We hypothesized that loss of p47(phox) subunit will result in decreased reactive oxygen species production and resistance to heart failure...
  9. doi request reprint Angiotensin-converting enzyme 2 suppresses pathological hypertrophy, myocardial fibrosis, and cardiac dysfunction
    Jiuchang Zhong
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada
    Circulation 122:717-28, 18 p following 728. 2010
    ..We hypothesized that ACE2 is a negative regulator of angiotensin II (Ang II)-mediated signaling and its adverse effects on the cardiovascular system...
  10. doi request reprint Angiotensin-converting enzyme 2 is a critical determinant of angiotensin II-induced loss of vascular smooth muscle cells and adverse vascular remodeling
    Vaibhav B Patel
    From the Division of Cardiology, Department of Medicine V B P, n p, M S M, G Y O, Mazankowski Alberta Heart Institute V B P, D F, R B, n p, S T D, Z K, G Y O, Department of Physiology D F, R B, S T D, Z K, G Y O, and Department of Obstetrics and Gynecology J S M, S T D, University of Alberta, Edmonton, Alberta, Canada State Key Laboratory of Medical Genomics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China J C Z and Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Shanghai, China J C Z
    Hypertension 64:157-64. 2014
    ..In conclusion, the key counter-regulatory role of ACE2 against an activated renin-angiotensin system provides novel insights into the role of ACE2 in vascular diseases. ..
  11. doi request reprint Angiotensin 1-7 ameliorates diabetic cardiomyopathy and diastolic dysfunction in db/db mice by reducing lipotoxicity and inflammation
    Jun Mori
    Department of Pediatrics, Department of Pharmacology, Mazankowski Alberta Heart Institute, Department of Physiology, and Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Canada
    Circ Heart Fail 7:327-39. 2014
    ..We studied the effects of Ang 1-7 on diabetic cardiomyopathy in db/db diabetic mice to elucidate the therapeutic effects and mechanism of action...
  12. pmc Loss of TIMP3 selectively exacerbates diabetic nephropathy
    Ratnadeep Basu
    Dept of Physiology, Univ of Alberta, Edmonton, Alberta, Canada T6G 2S2
    Am J Physiol Renal Physiol 303:F1341-52. 2012
    ..Our data provide definitive evidence for a critical and selective role of TIMP3 in diabetic renal injury consistent with gene expression findings from human diabetic kidneys...
  13. doi request reprint TIMP3 is the primary TIMP to regulate agonist-induced vascular remodelling and hypertension
    Ratnadeep Basu
    Department of Physiology, University of Alberta, 474 HMRC, Edmonton, Alberta, Canada T6G 2S2
    Cardiovasc Res 98:360-71. 2013
    ..In response to a hypertensive stimulus, the balance between MMPs and TIMPs is altered. We examined the role of TIMPs in agonist-induced hypertension...
  14. pmc Loss of angiotensin-converting enzyme-2 exacerbates diabetic cardiovascular complications and leads to systolic and vascular dysfunction: a critical role of the angiotensin II/AT1 receptor axis
    Vaibhav B Patel
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Alberta, Edmonton, Canada
    Circ Res 110:1322-35. 2012
    ..Angiotensin-converting enzyme-2 (ACE2) is a negative regulator of the renin-angiotensin system. We hypothesize that loss of ACE2 exacerbates cardiovascular complications induced by diabetes...
  15. doi request reprint TIMP2 deficiency accelerates adverse post-myocardial infarction remodeling because of enhanced MT1-MMP activity despite lack of MMP2 activation
    Vijay Kandalam
    Department of Physiology, Cardiovascular Research Centre, University of Alberta, Edmonton, Alberta, Canada
    Circ Res 106:796-808. 2010
    ..Hence, it is difficult to predict the function of TIMP2 as protective (MMP-inhibiting) or harmful (MMP-activating) in heart disease...
  16. doi request reprint Type 1 diabetic cardiomyopathy in the Akita (Ins2WT/C96Y) mouse model is characterized by lipotoxicity and diastolic dysfunction with preserved systolic function
    Ratnadeep Basu
    Department of Physiology, Rm 474, Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
    Am J Physiol Heart Circ Physiol 297:H2096-108. 2009
    ..We conclude that early type 1 diabetic cardiomyopathy is characterized by diastolic dysfunction associated with lipotoxic cardiomyopathy with preserved systolic function in the absence of interstitial fibrosis and hypertrophy...
  17. doi request reprint Tumor necrosis factor induces matrix metalloproteinases in cardiomyocytes and cardiofibroblasts differentially via superoxide production in a PI3Kgamma-dependent manner
    Ahmed E Awad
    Dept of Physiology, Univ of Alberta, 474 HMRC, Edmonton, AB T6G 2S2, Canada
    Am J Physiol Cell Physiol 298:C679-92. 2010
    ....
  18. pmc Loss of Timp3 gene leads to abdominal aortic aneurysm formation in response to angiotensin II
    Ratnadeep Basu
    Department of Physiology, Division of Cardiology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada
    J Biol Chem 287:44083-96. 2012
    ..Hence, replenishing TIMP3, a physiological inhibitor of a number of metalloproteinases, could serve as a therapeutic approach in limiting AAA development or expansion...
  19. doi request reprint Lack of tissue inhibitor of metalloproteinases 2 leads to exacerbated left ventricular dysfunction and adverse extracellular matrix remodeling in response to biomechanical stress
    Vijay Kandalam
    Assistant Professor, Department of Physiology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada
    Circulation 124:2094-105. 2011
    ..Tissue inhibitor of metalloproteinases 2 is unique among TIMPs in activating pro-MMP2 in addition to inhibiting a number of MMPs. Given this dual role of TIMP2, we investigated whether TIMP2 serves a critical role in heart disease...
  20. doi request reprint Agonist-induced hypertrophy and diastolic dysfunction are associated with selective reduction in glucose oxidation: a metabolic contribution to heart failure with normal ejection fraction
    Jun Mori
    Department of Pediatrics and Pharmacology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada
    Circ Heart Fail 5:493-503. 2012
    ....
  21. doi request reprint Heterozygote loss of ACE2 is sufficient to increase the susceptibility to heart disease
    Wang Wang
    Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, T6G 2S2, Canada
    J Mol Med (Berl) 92:847-58. 2014
    ..These changes occurred with increased renal fibrosis and superoxide production. Partial heterozygote loss of ACE2 is sufficient to increase the susceptibility to heart disease secondary to pressure overload and Ang II infusion...
  22. pmc Loss of Apelin exacerbates myocardial infarction adverse remodeling and ischemia-reperfusion injury: therapeutic potential of synthetic Apelin analogues
    Wang Wang
    Department of Physiology, University of Alberta, Edmonton, Alberta, Canada
    J Am Heart Assoc 2:e000249. 2013
    ..Coronary artery disease leading to myocardial ischemia is the most common cause of heart failure. Apelin (APLN), the endogenous peptide ligand of the APJ receptor, has emerged as a novel regulator of the cardiovascular system...
  23. pmc Human recombinant ACE2 reduces the progression of diabetic nephropathy
    Gavin Y Oudit
    Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
    Diabetes 59:529-38. 2010
    ..Inhibition of ACE2 function accelerates diabetic kidney injury, whereas renal ACE2 is downregulated in diabetic nephropathy. We examined the ability of human recombinant ACE2 (hrACE2) to slow the progression of diabetic kidney injury...
  24. doi request reprint MMP-2 mediates angiotensin II-induced hypertension under the transcriptional control of MMP-7 and TACE
    Jeffrey Odenbach
    Department of Biochemistry, School of Molecular and Systems Medicine, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 57:123-30. 2011
    ..This suggests a functional specialization of MMP-2 in agonist-induced cardiovascular disease development that has potential implications for the design of metalloproteinase-based therapeutic strategies...
  25. doi request reprint Angiotensin II induced proteolytic cleavage of myocardial ACE2 is mediated by TACE/ADAM-17: a positive feedback mechanism in the RAS
    Vaibhav B Patel
    Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Canada Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Canada
    J Mol Cell Cardiol 66:167-76. 2014
    ..In HF, elevated plasma ACE2 activity likely represents loss of the protective effects of ACE2 in the heart...
  26. doi request reprint Loss of angiotensin-converting enzyme 2 accelerates maladaptive left ventricular remodeling in response to myocardial infarction
    Zamaneh Kassiri
    Department of Physiology, University of Alberta, Edmonton, Canada
    Circ Heart Fail 2:446-55. 2009
    ..We hypothesized that ACE2 deficiency may compromise the cardiac response to myocardial infarction (MI)...
  27. doi request reprint Pressure-overload-induced heart failure induces a selective reduction in glucose oxidation at physiological afterload
    Pavel Zhabyeyev
    Division of Cardiology, Department of Medicine, University of Alberta, 8440 112 Street NW, Edmonton, AB, Canada T6G 2B7
    Cardiovasc Res 97:676-85. 2013
    ..Our aim is to characterize the changes in energy substrate metabolism associated with pressure overload and ischaemia-reperfusion (I/R) injury...
  28. doi request reprint Myocardial recovery from ischemia-reperfusion is compromised in the absence of tissue inhibitor of metalloproteinase 4
    Abhijit Takawale
    From the Department of Physiology A T, D F, R B, M S, W W, X W, G Y O, Z K and Department of Medicine Division of Cardiology N P, G Y O, University of Alberta, Edmonton, Alberta, Canada and Mazankowski Alberta Heart Institute, Edmonton, Alberta, Canada A T, D F, R B, M S, n p, W W, X W, G Y O, Z K
    Circ Heart Fail 7:652-62. 2014
    ..TIMP4 levels are reduced in myocardial infarction; however, its causal role in progression of post-I/R injury has not been explored...
  29. doi request reprint Tissue inhibitor of metalloproteinases (TIMPs) in heart failure
    Linn Moore
    Department of Physiology, Cardiovascular Research Centre, Mazankowski Alberta Heart Institute, University of Alberta, Heritage Medical Research Centre, Edmonton, AB, Canada
    Heart Fail Rev 17:693-706. 2012
    ..We will further discuss how ECM molecules and regulatory genes can be used as biomarkers of disease in heart failure patients...
  30. doi request reprint TIMP2 and TIMP3 have divergent roles in early renal tubulointerstitial injury
    Zuocheng Wang
    1 Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada 2 Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Kidney Int 85:82-93. 2014
    ..Thus, TIMP2 and TIMP3 play differential and contrasting roles in renal injury: TIMP3 protects from damage, whereas TIMP2 promotes injury through MMP2 activation. ..
  31. doi request reprint PI3Kα is essential for the recovery from Cre/tamoxifen cardiotoxicity and in myocardial insulin signalling but is not required for normal myocardial contractility in the adult heart
    Brent A McLean
    Department of Physiology, University of Alberta, Edmonton, Alberta, Canada Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Cardiovasc Res 105:292-303. 2015
    ..Here we seek to clarify the role of PI3Kα in normal heart physiology and investigate changes in related signalling pathways...
  32. doi request reprint Divergent roles of matrix metalloproteinase 2 in pathogenesis of thoracic aortic aneurysm
    Mengcheng Shen
    From the Department of Physiology, University of Alberta, Edmonton, Alberta, Canada and Cardiovascular Research Center, Mazankowski Alberta Heart Institute, Edmonton, Alberta, Canada
    Arterioscler Thromb Vasc Biol 35:888-98. 2015
    ..MMP2 has been associated with aneurysm in patients and in animal models. We investigated the role of MMP2 in thoracic aortic aneurysm using 2 models of aortic remodeling and aneurysm...
  33. doi request reprint Matrix metalloproteinase-7 and ADAM-12 (a disintegrin and metalloproteinase-12) define a signaling axis in agonist-induced hypertension and cardiac hypertrophy
    Xiang Wang
    Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada
    Circulation 119:2480-9. 2009
    ..Here, we report that matrix metalloproteinase-7 (MMP-7) and a disintegrin and metalloproteinase-12 (ADAM-12) form a novel signaling axis in these processes...
  34. doi request reprint Gender-dependent aortic remodelling in patients with bicuspid aortic valve-associated thoracic aortic aneurysm
    Jiwon Lee
    Department of Physiology, University of Alberta, Edmonton, AB, T6G 2S2, Canada
    J Mol Med (Berl) 92:939-49. 2014
    ..Lower smooth muscle cell density in the medial layer of aortas from males with BAV-TAA samples corresponded to the increased caspase-3 cleavage compared to that of females...
  35. doi request reprint Matrix metalloproteinase-2 mediates a mechanism of metabolic cardioprotection consisting of negative regulation of the sterol regulatory element-binding protein-2/3-hydroxy-3-methylglutaryl-CoA reductase pathway in the heart
    Xiang Wang
    From the Departments of Biochemistry X W, E B, S H A, C F P and Physiology A T, Z K, Mazankowski Alberta Heart Institute Z K, C F P, Cardiovascular Research Group Z K, C F P, and Faculty of Medicine and Dentistry X W, E B, S H A, C F P, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 65:882-8. 2015
    ..This complex phenotype is, at least in part, because of the cardiac sterol regulatory element-binding protein-2/3-hydroxy-3-methylglutaryl-coenzyme A reductase pathway being upregulated in MMP-2 deficiency. ..
  36. pmc Titin is a target of matrix metalloproteinase-2: implications in myocardial ischemia/reperfusion injury
    Mohammad A M Ali
    Department of Pharmacology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    Circulation 122:2039-47. 2010
    ..Here we determine whether titin is an intracellular substrate for MMP-2 and if its degradation during ischemia/reperfusion contributes to cardiac contractile dysfunction...
  37. pmc Circulating levels of tumor necrosis factor-alpha receptor 2 are increased in heart failure with preserved ejection fraction relative to heart failure with reduced ejection fraction: evidence for a divergence in pathophysiology
    Brendan N Putko
    Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada
    PLoS ONE 9:e99495. 2014
    ..Inflammation in response to comorbid conditions, such as hypertension and diabetes, may play a proportionally larger role in HFPEF as compared to HF with reduced ejection fraction (HFREF)...
  38. doi request reprint Extracellular matrix communication and turnover in cardiac physiology and pathology
    Abhijit Takawale
    Department of Physiology, University of Alberta, Cardiovascular Research Centre, Mazankowski Alberta Heart Institute, Edmonton, Alberta, Canada
    Compr Physiol 5:687-719. 2015
    ..2015 American Physiological Society. Compr Physiol 5: 687-719, 2015. ..
  39. doi request reprint Matrix as an interstitial transport system
    Dong Fan
    From the Department of Physiology, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada D F, Z K and Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands E E C
    Circ Res 114:889-902. 2014
    ..The information summarized and discussed here are not limited to the cardiovascular ECM but encompass ECM in general with specific references to the cardiovascular system. ..
  40. doi request reprint Uncoupling between enhanced excitation-contraction coupling and the response to heart disease: lessons from the PI3Kγ knockout murine model
    Danny Guo
    Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, Canada
    J Mol Cell Cardiol 50:606-12. 2011
    ....
  41. pmc The Alberta Heart Failure Etiology and Analysis Research Team (HEART) study
    Justin A Ezekowitz
    Mazankowski Alberta Heart Institute, 2C2 WMC, 8440 112 Street, Edmonton, AB, Canada
    BMC Cardiovasc Disord 14:91. 2014
    ..The current one-year mortality rate after diagnosis of heart failure remains high at >25%. Consequently, new therapeutic strategies need to be developed for this debilitating condition...
  42. doi request reprint Tumor necrosis factor-alpha-converting enzyme is a key regulator of agonist-induced cardiac hypertrophy and fibrosis
    Xiang Wang
    Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada
    Hypertension 54:575-82. 2009
    ..Targeting TACE has potential therapeutic importance for modulating agonist-induced cardiac remodeling...
  43. doi request reprint Antenatal sildenafil treatment attenuates pulmonary hypertension in experimental congenital diaphragmatic hernia
    Christina Luong
    Department of Pediatrics, Women and Children Health Research Institute, Cardiovascular Research Group, University of Alberta, Edmonton, Canada
    Circulation 123:2120-31. 2011
    ..Because of the limited success in postnatal management of CDH, we hypothesized that antenatal PDE5 inhibition would attenuate pulmonary artery remodeling in experimental nitrofen-induced CDH...
  44. ncbi request reprint Reduction of I(to) causes hypertrophy in neonatal rat ventricular myocytes
    Zamaneh Kassiri
    Department of Physiology, Heart and Stroke Richard Lewar Center, University of Toronto, Toronto, Canada
    Circ Res 90:578-85. 2002
    ..2)N infection were prevented by blocking Ca2+ entry and excitability with verapamil or high [K+]o. Our studies suggest that reductions of K(v4.2/3)-based I(to) play a role in hypertrophy signaling by activation of calcineurin...
  45. ncbi request reprint Role of PI3 kinase gamma in excitation-contraction coupling and heart disease
    Gavin Y Oudit
    Department of Medicine, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada
    Cardiovasc Hematol Disord Drug Targets 7:295-304. 2007
    ..In this review article, we discuss the key role of PI3Kgamma gamma in regulating cAMP, Ca(2+) cycling, beta-adrenergic signaling and myocardial structure and function in heart disease...