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Aged‐senescent cells contribute to impaired heart regeneration

Aging cell, 2019-06, Vol.18 (3), p.e12931-n/a

2019

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Cardioprotective actions by a water-soluble carbon monoxide-releasing molecule

Circulation research, 2003-07, Vol.93 (2), p.e2-e8

2003

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Transplantation of Skeletal Muscle-Derived Sca-1 + /PW1 + /Pax7 - Interstitial Cells (PICs) Improves Cardiac Function and Attenuates Remodeling in Mice Subjected to Myocardial Infarction

Cells (Basel, Switzerland), 2022-12, Vol.11 (24), p.4050

2022

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Transient Receptor Potential Canonical 5 (TRPC5): Regulation of Heart Rate and Protection against Pathological Cardiac Hypertrophy

Biomolecules (Basel, Switzerland), 2024-04, Vol.14 (4), p.442

2024

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A Novel α-Calcitonin Gene-Related Peptide Analogue Protects Against End-Organ Damage in Experimental Hypertension, Cardiac Hypertrophy, and Heart Failure

Circulation (New York, N.Y.), 2017-07, Vol.136 (4), p.367-383

2017

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The Role of RIP2 in p38 MAPK Activation in the Stressed Heart

The Journal of biological chemistry, 2008-05, Vol.283 (18), p.11964-11971

2008

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p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin

The FASEB journal, 2019-12, Vol.33 (12), p.13131-13144

2019

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Overexpression of the transcription factor Hand1 causes predisposition towards arrhythmia in mice

Journal of molecular and cellular cardiology, 2009-07, Vol.47 (1), p.133-141

2009

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Measuring left ventricular function in the normal, infarcted and CORM-3-preconditioned mouse heart using complex admittance-derived pressure volume loops

Journal of pharmacological and toxicological methods, 2009-03, Vol.59 (2), p.94-99

2009

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Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing

Nature communications, 2013, Vol.4 (1), p.2081-2081, Article 2081

2013

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The POU4F2/Brn-3b transcription factor is required for the hypertrophic response to angiotensin II in the heart

Cell death & disease, 2019-08, Vol.10 (8), p.621-18, Article 621

2019

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Advancements in pressure–volume catheter technology – stress remodelling after infarction

Experimental physiology, 2013-03, Vol.98 (3), p.614-621

2013

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Glycogen Synthase Kinase-3 Inactivation Is Not Required for Ischemic Preconditioning or Postconditioning in the Mouse

Circulation research, 2008-08, Vol.103 (3), p.307-314

2008

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Myocardial stress remodelling after regional infarction is independent of glycogen synthase kinase-3 inactivation

Journal of molecular and cellular cardiology, 2010-11, Vol.49 (5), p.897-900

2010

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Characterization of the phospholemman knockout mouse heart: depressed left ventricular function with increased Na-K-ATPase activity

American journal of physiology. Heart and circulatory physiology, 2008-02, Vol.294 (2), p.H613-H621

2008

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Macrophage scavenger receptor 1 mediates lipid-induced inflammation in non-alcoholic fatty liver disease

Journal of hepatology, 2022-05, Vol.76 (5), p.1001-1012

2022

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Reperfusion kinase phosphorylation is essential but not sufficient in the mediation of pharmacological preconditioning : Characterisation in the bi-phasic profile of early and late protection

Cardiovascular research, 2007, Vol.73 (1), p.153-163

2007

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MAPKAPK-2 Modulates p38-MAPK Localization and Small Heat Shock Protein Phosphorylation but Does Not Mediate the Injury Associated with p38-MAPK Activation during Myocardial Ischemia

Cell stress & chaperones, 2009-09, Vol.14 (5), p.477-489

2009

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Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)

Cardiovascular research, 2007-06, Vol.74 (3), p.466-470

2007

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Cardioprotection initiated by reactive oxygen species is dependent on activation of PKCepsilon

American journal of physiology. Heart and circulatory physiology, 2006-10, Vol.291 (4), p.H1893-H1899

2006

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The activation of p38 alpha, and not p38 beta, mitogen-activated protein kinase is required for ischemic preconditioning

Journal of molecular and cellular cardiology, 2010-06, Vol.48 (6), p.1324-1328

2010

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Constitutive glycogen synthase kinase-3alpha/beta activity protects against chronic beta-adrenergic remodelling of the heart

Cardiovascular research, 2010-08, Vol.87 (3), p.494-503

2010

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A chemical genetic approach reveals that p38alpha MAPK activation by diphosphorylation aggravates myocardial infarction and is prevented by the direct binding of SB203580

The Journal of biological chemistry, 2010-01, Vol.285 (5), p.2968-2975

2010

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Rate of red cell production in two nephrectomized patients

Archives of internal medicine (1960), 1968-09, Vol.122 (3), p.230

1968

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Validating Eaton's Hypothesis: Cubane as a Benzene Bioisostere

Angewandte Chemie (International ed.), 2016-03, Vol.55 (11), p.3580-3585

International ed. in English, 2016

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Aged‐senescent cells contribute to impaired heart regeneration

Cardioprotective actions by a water-soluble carbon monoxide-releasing molecule

Transplantation of Skeletal Muscle-Derived Sca-1 + /PW1 + /Pax7 - Interstitial Cells (PICs) Improves Cardiac Function and Attenuates Remodeling in Mice Subjected to Myocardial Infarction

Transient Receptor Potential Canonical 5 (TRPC5): Regulation of Heart Rate and Protection against Pathological Cardiac Hypertrophy

A Novel α-Calcitonin Gene-Related Peptide Analogue Protects Against End-Organ Damage in Experimental Hypertension, Cardiac Hypertrophy, and Heart Failure

The Role of RIP2 in p38 MAPK Activation in the Stressed Heart

p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin

Overexpression of the transcription factor Hand1 causes predisposition towards arrhythmia in mice

Measuring left ventricular function in the normal, infarcted and CORM-3-preconditioned mouse heart using complex admittance-derived pressure volume loops

Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing

The POU4F2/Brn-3b transcription factor is required for the hypertrophic response to angiotensin II in the heart

Advancements in pressure–volume catheter technology – stress remodelling after infarction

Glycogen Synthase Kinase-3 Inactivation Is Not Required for Ischemic Preconditioning or Postconditioning in the Mouse

Myocardial stress remodelling after regional infarction is independent of glycogen synthase kinase-3 inactivation

Characterization of the phospholemman knockout mouse heart: depressed left ventricular function with increased Na-K-ATPase activity

Macrophage scavenger receptor 1 mediates lipid-induced inflammation in non-alcoholic fatty liver disease

Reperfusion kinase phosphorylation is essential but not sufficient in the mediation of pharmacological preconditioning : Characterisation in the bi-phasic profile of early and late protection

MAPKAPK-2 Modulates p38-MAPK Localization and Small Heat Shock Protein Phosphorylation but Does Not Mediate the Injury Associated with p38-MAPK Activation during Myocardial Ischemia

Post-infarction remodeling is independent of mitogen-activated protein kinase kinase 3 (MKK3)

Cardioprotection initiated by reactive oxygen species is dependent on activation of PKCepsilon

The activation of p38 alpha, and not p38 beta, mitogen-activated protein kinase is required for ischemic preconditioning

Constitutive glycogen synthase kinase-3alpha/beta activity protects against chronic beta-adrenergic remodelling of the heart

A chemical genetic approach reveals that p38alpha MAPK activation by diphosphorylation aggravates myocardial infarction and is prevented by the direct binding of SB203580

Rate of red cell production in two nephrectomized patients

Validating Eaton's Hypothesis: Cubane as a Benzene Bioisostere

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