Mechanisms of Sex Differences in TNFR2-Mediated Cardioprotection | Zendy

Meijing Wang | Zendy; Paul R. Crisostomo | Zendy; Troy A. Markel | Zendy; Yue Wang | Zendy; Daniel R. Meldrum | Zendy

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Mechanisms of Sex Differences in TNFR2-Mediated Cardioprotection

Author(s) -

Meijing Wang,

Paul R. Crisostomo,

Troy A. Markel,

Yue Wang,

Daniel R. Meldrum

Publication year - 2008

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.107.756890

Subject(s) - cardioprotection , medicine , ischemia , knockout mouse , endocrinology , reperfusion injury , socs3 , stat3 , signal transduction , receptor , microbiology and biotechnology , biology , cancer , suppressor

TNFR1/TNFR2 signaling may mediate different cellular and molecular responses (injury versus protection) and the balance may be affected by sex hormones. Previous studies have shown that females have improved myocardial functional recovery, TNFR1 signaling resistance, and increased SOCS3 expression after acute ischemia/reperfusion when compared with males. However, it is unknown whether the TNFR2 pathway protects the myocardium from ischemia/reperfusion injury, and if so, whether sex differences exist in TNFR2-mediated cardioprotection. Therefore, we hypothesized that (1) TNFR2 mediates myocardial protection from ischemia/reperfusion through STAT3, SOCS3, and vascular endothelial growth factor in both sexes; and (2) TNFR2 elicits greater protective signaling in females compared with males.

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