Estrogen Receptor β Agonism Increases Survival in Experimentally Induced Sepsis and Ameliorates the Genomic Sepsis Signature: A Pharmacogenomic Study
Author(s) -
Eirini Christaki,
Steven M. Opal,
James C. Keith,
Nubar Kessinian,
John E. Palardy,
Nicolas A. Parejo,
Edward R. LaVallie,
Lisa Racie,
William Mounts,
Michael S. Malamas,
Richard E. Mewshaw,
Heather A. Harris,
George P. Vlasuk
Publication year - 2010
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/651276
Subject(s) - sepsis , biology , agonist , proinflammatory cytokine , estrogen receptor , transcriptome , estrogen receptor alpha , receptor , estrogen , pharmacology , cancer research , immunology , medicine , inflammation , gene expression , endocrinology , gene , cancer , breast cancer , biochemistry
Nonsteroidal agonists have been developed that selectively bind to and activate estrogen receptor beta (ERbeta) rather than estrogen receptor alpha (ERalpha). ERbeta is expressed equally in both male and female mammals in multiple extragonadal tissues. Work reported elsewhere has demonstrated that ERbeta agonists have beneficial effects in multiple (but not all) models of inflammatory diseases and also increase survival in experimentally induced sepsis.
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