TY - JOUR
T1 - Eicosanoids derived from cytochrome P450 pathway of arachidonic acid and inflammatory shock
AU - Tunctan, Bahar
AU - Senol, Sefika Pinar
AU - Temiz-Resitoglu, Meryem
AU - Guden, Demet Sinem
AU - Sahan-Firat, Seyhan
AU - Falck, John R.
AU - Malik, Kafait U.
N1 - Funding Information:
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Our studies presented in this review were supported in part by grants from Mersin University (BAP ECZ F EMB [KB] 2003-1, BAP ECZF EMB [BT] 2004-3, BAP ECZF EMB [BT] 2006-3, BAP SBE EMB [RBK] 2006-3 DR, BAP SBE EMB [TC] 2008-6 DR, BAP-ECZ F FB [BT] 2010-5 B, BAP SBE F [MK] 2011-5 YL, BAP-SBE EMBB [ANS] 2012-4 DR, BAP-ECZ F EMBF [SŞF] 2012-6 B, BAP-SBE FB [SPS] 2014-3 YL, and 2015-AP3-1343), Novartis Turkey, TUBITAK (SBAG-106S299, SBAG-109S121, and SBAG-215S679), USPHS NIH (R01HL139793), and the Robert A. Welch Foundation (I-0011).
Funding Information:
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Our studies presented in this review were supported in part by grants from Mersin University (BAP ECZ F EMB [KB] 2003-1, BAP ECZF EMB [BT] 2004-3, BAP ECZF EMB [BT] 2006-3, BAP SBE EMB [RBK] 2006-3 DR, BAP SBE EMB [TC] 2008-6 DR, BAP-ECZ F FB [BT] 2010-5 B, BAP SBE F [MK] 2011-5 YL, BAP-SBE EMBB [ANS] 2012-4 DR, BAP-ECZ F EMBF [S?F] 2012-6 B, BAP-SBE FB [SPS] 2014-3 YL, and 2015-AP3-1343), Novartis Turkey, TUBITAK (SBAG-106S299, SBAG-109S121, and SBAG-215S679), USPHS NIH (R01HL139793), and the Robert A. Welch Foundation (I-0011).
Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2019/12
Y1 - 2019/12
N2 - Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock, the most common form of vasodilatory shock, is a subset of sepsis in which circulatory and cellular/metabolic abnormalities are severe enough to increase mortality. Inflammatory shock constitutes the hallmark of sepsis, but also a final common pathway of any form of severe long-term tissue hypoperfusion. The pathogenesis of inflammatory shock seems to be due to circulating substances released by pathogens (e.g., bacterial endotoxins) and host immuno-inflammatory responses (e.g., changes in the production of histamine, bradykinin, serotonin, nitric oxide [NO], reactive nitrogen and oxygen species, and arachidonic acid [AA]-derived eicosanoids mainly through NO synthase, cyclooxygenase, and cytochrome P450 [CYP] pathways, and proinflammatory cytokine formation). Therefore, refractory hypotension to vasoconstrictors with end-organ hypoperfusion is a life threatening feature of inflammatory shock. This review summarizes the current knowledge regarding the role of eicosanoids derived from CYP pathway of AA in animal models of inflammatory shock syndromes with an emphasis on septic shock in addition to potential therapeutic strategies targeting specific CYP isoforms responsible for proinflammatory/anti-inflammatory mediator production.
AB - Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock, the most common form of vasodilatory shock, is a subset of sepsis in which circulatory and cellular/metabolic abnormalities are severe enough to increase mortality. Inflammatory shock constitutes the hallmark of sepsis, but also a final common pathway of any form of severe long-term tissue hypoperfusion. The pathogenesis of inflammatory shock seems to be due to circulating substances released by pathogens (e.g., bacterial endotoxins) and host immuno-inflammatory responses (e.g., changes in the production of histamine, bradykinin, serotonin, nitric oxide [NO], reactive nitrogen and oxygen species, and arachidonic acid [AA]-derived eicosanoids mainly through NO synthase, cyclooxygenase, and cytochrome P450 [CYP] pathways, and proinflammatory cytokine formation). Therefore, refractory hypotension to vasoconstrictors with end-organ hypoperfusion is a life threatening feature of inflammatory shock. This review summarizes the current knowledge regarding the role of eicosanoids derived from CYP pathway of AA in animal models of inflammatory shock syndromes with an emphasis on septic shock in addition to potential therapeutic strategies targeting specific CYP isoforms responsible for proinflammatory/anti-inflammatory mediator production.
KW - Animal models
KW - Arachidonic acid
KW - CYP-derived eicosanoids
KW - Inflammatory shock
KW - Septic shock
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U2 - 10.1016/j.prostaglandins.2019.106377
DO - 10.1016/j.prostaglandins.2019.106377
M3 - Review article
C2 - 31586592
AN - SCOPUS:85073024119
SN - 1098-8823
VL - 145
JO - Prostaglandins and Other Lipid Mediators
JF - Prostaglandins and Other Lipid Mediators
M1 - 106377
ER -