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Oxidized phospholipids in Doxorubicin-induced cardiotoxicity

Chemico-biological interactions, 2019-04, Vol.303, p.35-39

2019

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SKI activates the Hippo pathway via LIMD1 to inhibit cardiac fibroblast activation

Basic research in cardiology, 2021-04, Vol.116 (1), p.25, Article 25

2021

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High molecular weight fibroblast growth factor-2 in the human heart is a potential target for prevention of cardiac remodeling

PloS one, 2014-05, Vol.9 (5), p.e97281-e97281

2014

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Elimination or neutralization of endogenous high-molecular-weight FGF2 mitigates doxorubicin-induced cardiotoxicity

American journal of physiology. Heart and circulatory physiology, 2019-02, Vol.316 (2), p.H279-H288

2019

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Connexin 43 phosphorylation and degradation are required for adipogenesis

Biochimica et biophysica acta, 2012-10, Vol.1823 (10), p.1731-1744

2012

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Phosphorylation of serine 262 in the gap junction protein connexin-43 regulates DNA synthesis in cell-cell contact forming cardiomyocytes

Journal of cell science, 2004-01, Vol.117 (Pt 3), p.507-514

2004

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A Cardiac Mitochondrial FGFR1 Mediates the Antithetical Effects of FGF2 Isoforms on Permeability Transition

Cells (Basel, Switzerland), 2021-10, Vol.10 (10), p.2735

2021

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Preferential accumulation and export of high molecular weight FGF-2 by rat cardiac non-myocytes

Cardiovascular research, 2011-01, Vol.89 (1), p.139-147

2011

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Non-mitogenic FGF2 protects cardiomyocytes from acute doxorubicin-induced toxicity independently of the protein kinase CK2/heme oxygenase-1 pathway

Cell and tissue research, 2018-12, Vol.374 (3), p.607-617

2018

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Elimination of endogenous high molecular weight FGF2 prevents pressure-overload-induced systolic dysfunction, linked to increased FGFR1 activity and NR1D1 expression

Cell and tissue research, 2021-09, Vol.385 (3), p.753-768

2021

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Fibroblast growth factor-2-mediated protection of cardiomyocytes from the toxic effects of doxorubicin requires the mTOR/Nrf-2/HO-1 pathway

Oncotarget, 2017-10, Vol.8 (50), p.87415-87430

2017

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Chromatin compaction and cell death by high molecular weight FGF-2 depend on its nuclear localization, intracrine ERK activation, and engagement of mitochondria

Journal of cellular physiology, 2007-12, Vol.213 (3), p.690-698

2007

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Basic Fibroblast Growth Factor in Atria and Ventricles of the Vertebrate Heart

The Journal of cell biology, 1989-10, Vol.109 (4), p.1865-1875

1989

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Ischemia-induced dephosphorylation of cardiomyocyte connexin-43 is reduced by okadaic acid and calyculin A but not fostriecin

Molecular and cellular biochemistry, 2003-01, Vol.242 (1-2), p.129-134

2003

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THE CARDIOPROTECTIVE ROLE OF NACA IN THE PREVENTION OF DOXORUBICIN AND TRASTUZUMAB MEDIATED CARDIAC DYSFUNCTION

Canadian journal of cardiology, 2014-10, Vol.30 (10), p.S126-S127

2014

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Overexpression of FGF-2 increases cardiac myocyte viability after injury in isolated mouse hearts

American journal of physiology. Heart and circulatory physiology, 2001-03, Vol.280 (3), p.H1039-H1050

2001

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Prenatal exposure to maternal low protein diet suppresses replicative potential of myocardial cells

Nutrition, metabolism, and cardiovascular diseases, 2009-12, Vol.19 (10), p.707-712

2009

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Overexpression of long or short FGFR-1 results in FGF-2-mediated proliferation in neonatal cardiac myocyte cultures

Cardiovascular research, 1999-06, Vol.42 (3), p.696-705

1999

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Administration of FGF-2 to the Heart Stimulates Connexin-43 Phosphorylation at Protein Kinase C Target Sites

Cell communication & adhesion, 2006, Vol.13 (1-2), p.13-19

2006

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Trends in Steelmaking 2012

Transactions of the Indian Institute of Metals, 2013-12, Vol.66 (5-6), p.561-566

2013

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High- but not low-molecular weight FGF-2 causes cardiac hypertrophy in vivo ; possible involvement of cardiotrophin-1

Journal of molecular and cellular cardiology, 2007-01, Vol.42 (1), p.222-233

2007

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Inhibition of TGFβ signaling potentiates the FGF-2-induced stimulation of cardiomyocyte DNA synthesis

Cardiovascular research, 2004-12, Vol.64 (3), p.516-525

2004

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Mineral liberation by particle bed breakage

Minerals engineering, 1997-02, Vol.10 (2), p.175-187

1997

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Adult cardiomyocytes express functional high-affinity receptors for basic fibroblast growth factor

American journal of physiology. Heart and circulatory physiology, 1995-05, Vol.268 (5), p.H1927-H1938

1995

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The CSIRO Hopkinson Bar Facility for large diameter particle breakage

Minerals engineering, 1998-09, Vol.11 (9), p.861-869

1998

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Oxidized phospholipids in Doxorubicin-induced cardiotoxicity

SKI activates the Hippo pathway via LIMD1 to inhibit cardiac fibroblast activation

High molecular weight fibroblast growth factor-2 in the human heart is a potential target for prevention of cardiac remodeling

Elimination or neutralization of endogenous high-molecular-weight FGF2 mitigates doxorubicin-induced cardiotoxicity

Connexin 43 phosphorylation and degradation are required for adipogenesis

Phosphorylation of serine 262 in the gap junction protein connexin-43 regulates DNA synthesis in cell-cell contact forming cardiomyocytes

A Cardiac Mitochondrial FGFR1 Mediates the Antithetical Effects of FGF2 Isoforms on Permeability Transition

Preferential accumulation and export of high molecular weight FGF-2 by rat cardiac non-myocytes

Non-mitogenic FGF2 protects cardiomyocytes from acute doxorubicin-induced toxicity independently of the protein kinase CK2/heme oxygenase-1 pathway

Elimination of endogenous high molecular weight FGF2 prevents pressure-overload-induced systolic dysfunction, linked to increased FGFR1 activity and NR1D1 expression

Fibroblast growth factor-2-mediated protection of cardiomyocytes from the toxic effects of doxorubicin requires the mTOR/Nrf-2/HO-1 pathway

Chromatin compaction and cell death by high molecular weight FGF-2 depend on its nuclear localization, intracrine ERK activation, and engagement of mitochondria

Basic Fibroblast Growth Factor in Atria and Ventricles of the Vertebrate Heart

Ischemia-induced dephosphorylation of cardiomyocyte connexin-43 is reduced by okadaic acid and calyculin A but not fostriecin

THE CARDIOPROTECTIVE ROLE OF NACA IN THE PREVENTION OF DOXORUBICIN AND TRASTUZUMAB MEDIATED CARDIAC DYSFUNCTION

Overexpression of FGF-2 increases cardiac myocyte viability after injury in isolated mouse hearts

Prenatal exposure to maternal low protein diet suppresses replicative potential of myocardial cells

Overexpression of long or short FGFR-1 results in FGF-2-mediated proliferation in neonatal cardiac myocyte cultures

Administration of FGF-2 to the Heart Stimulates Connexin-43 Phosphorylation at Protein Kinase C Target Sites

Trends in Steelmaking 2012

High- but not low-molecular weight FGF-2 causes cardiac hypertrophy in vivo ; possible involvement of cardiotrophin-1

Inhibition of TGFβ signaling potentiates the FGF-2-induced stimulation of cardiomyocyte DNA synthesis

Mineral liberation by particle bed breakage

Adult cardiomyocytes express functional high-affinity receptors for basic fibroblast growth factor

The CSIRO Hopkinson Bar Facility for large diameter particle breakage

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