Gene Deletion of Protein Tyrosine Phosphatase 1B Protects Against Sepsis-Induced Cardiovascular Dysfunction and Mortality | Zendy

David Coquerel | Zendy; Rémi Névière | Zendy; Eugénie Delile | Zendy; Paul Mulder | Zendy; Xavier Maréchal | Zendy; David Montaigne | Zendy; Sylvanie Renet | Zendy; Isabelle RémyJouet | Zendy; Élodie Gomez | Zendy; JeanPaul Henry | Zendy; JeanClaude do Rego | Zendy; Vincent Richard | Zendy; Fabienne Tamion | Zendy

Open Access

Gene Deletion of Protein Tyrosine Phosphatase 1B Protects Against Sepsis-Induced Cardiovascular Dysfunction and Mortality

Author(s) -

David Coquerel,

Rémi Névière,

Eugénie Delile,

Paul Mulder,

Xavier Maréchal,

David Montaigne,

Sylvanie Renet,

Isabelle RémyJouet,

Élodie Gomez,

JeanPaul Henry,

JeanClaude do Rego,

Vincent Richard,

Fabienne Tamion

Publication year - 2014

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.114.303450

Subject(s) - sepsis , endothelial dysfunction , nitric oxide synthase , medicine , endocrinology , tyrosine phosphorylation , biology , pharmacology , immunology , nitric oxide , receptor

Cardiovascular dysfunction is a major cause of mortality in patients with sepsis. Recently, we showed that gene deletion or pharmacological inhibition of protein tyrosine phosphatase 1B (PTP1B) improves endothelial dysfunction and reduces the severity of experimental heart failure. However, the cardiovascular effect of PTP1B invalidation in sepsis is unknown. Thus, we explored the beneficial therapeutic effect of PTP1B gene deletion on lipopolysaccharide (LPS)-induced cardiovascular dysfunction, inflammation, and mortality.

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