Interleukin-13 Deficiency Aggravates Healing and Remodeling in Male Mice After Experimental Myocardial Infarction | Zendy

Ulrich Hofmann | Zendy; Susanne Knörr | Zendy; Benjamin Vogel | Zendy; Johannes Weirather | Zendy; Anna Frey | Zendy; Georg Ertl | Zendy; Stefan Frantz | Zendy

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Interleukin-13 Deficiency Aggravates Healing and Remodeling in Male Mice After Experimental Myocardial Infarction

Author(s) -

Ulrich Hofmann,

Susanne Knörr,

Benjamin Vogel,

Johannes Weirather,

Anna Frey,

Georg Ertl,

Stefan Frantz

Publication year - 2014

Publication title -

circulation heart failure

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.352

H-Index - 104

eISSN - 1941-3297

pISSN - 1941-3289

DOI - 10.1161/circheartfailure.113.001020

Subject(s) - wound healing , myocardial infarction , ligation , medicine , monocyte , ventricular remodeling , interleukin , inflammation , infiltration (hvac) , immunity , andrology , endocrinology , immunology , cytokine , immune system , thermodynamics , physics

Activation of innate immunity, especially infiltration of monocytes, is critical for proper wound healing and scar formation after myocardial infarction (MI). Therefore, we tested the hypothesis that interleukin-13 (IL-13), which influences the differentiation of monocytes/macrophages and has profibrotic properties, modulates wound healing and remodeling after MI.

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