Absence of thrombospondin-2 increases cardiomyocyte damage and matrix disruption in doxorubicin-induced cardiomyopathy (Q84222990)

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title

Absence of thrombospondin-2 increases cardiomyocyte damage and matrix disruption in doxorubicin-induced cardiomyopathy (English)

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3

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Blanche Louise Maria Schroen

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9

object named as

Blanche Schroen

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Peter Carmeliet

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author name string

Geert C van Almen

1

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Melissa Swinnen

2

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Wouter Verhesen

4

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Jack P M Cleutjens

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Jan D'hooge

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Fons K Verheyen

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Yigal M Pinto

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Stephane Heymans

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publication date

23 May 2011

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Journal of Molecular and Cellular Cardiology

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published in

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volume

51

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issue

3

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page(s)

318-328

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Preventive cardioprotection of erythropoietin against doxorubicin-induced cardiomyopathy

2 February 2020

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Erythropoietin protects against doxorubicin-induced cardiomyopathy via a phosphatidylinositol 3-kinase-dependent pathway

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Increased and prolonged inflammation and angiogenesis in delayed-type hypersensitivity reactions elicited in the skin of thrombospondin-2--deficient mice

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Thrombospondin-2: a potent endogenous inhibitor of tumor growth and angiogenesis

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Thrombospondin-2 Is Essential for Myocardial Matrix Integrity: Increased Expression Identifies Failure-Prone Cardiac Hypertrophy

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Absence of Thrombospondin-2 Causes Age-Related Dilated Cardiomyopathy

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Mice that lack the angiogenesis inhibitor, thrombospondin 2, mount an altered foreign body reaction characterized by increased vascularity

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C-phycocyanin ameliorates doxorubicin-induced oxidative stress and apoptosis in adult rat cardiomyocytes.

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Distinctive regulation and function of PI 3K/Akt and MAPKs in doxorubicin-induced apoptosis of human lung adenocarcinoma cells

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Identifiers

DOI

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2 February 2020

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