Protectins and maresins: New pro-resolving families of mediators in acute inflammation and resolution bioactive metabolome.
Protectins and maresins: New pro-resolving families of mediators in acute inflammation and resolution bioactive metabolome.
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DOI:
10.1016/j.bbalip.2014.08.006
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发表时间:
2015-04
期刊:
影响因子:
--
通讯作者:
Chiang N
中科院分区:
文献类型:
--
作者:
Serhan CN;Dalli J;Colas RA;Winkler JW;Chiang N
Acute inflammatory responses are protective, yet without timely resolution can lead to chronic inflammation and organ fibrosis. A systems approach to investigate self-limited (self-resolving) inflammatory exudates in mice and structural elucidation uncovered novel resolution phase mediators in vivo that stimulate endogenous resolution mechanisms in inflammation. Resolving inflammatory exudates and human leukocytes utilize DHA and other n-3 EFA to produce three structurally distinct families of potent di- and trihydroxy-containing products, with several stereospecific potent mediators in each family. Given their potent and stereoselective picogram actions, specific members of these new families of mediators from the DHA metabolome were named D-series resolvins (Resolvin D1 to Resolvin D6), protectins (including protectin D1-neuroprotectin D1), and maresins (MaR1 and MaR2). In this review, we focus on a) biosynthesis of protectins and maresins as anti-inflammatory - pro-resolving mediators; b) their complete stereochemical assignments and actions in vivo in disease models. Each pathway involves the biosynthesis of epoxide-containing intermediates produced from hydroperoxy-containing precursors from human leukocytes and within exudates. Also, aspirin triggers an endogenous DHA metabolome that biosynthesizes potent products in inflammatory exudates and human leukocytes, namely aspirin-triggered Neuroprotectin D1/Protectin D1 [AT-(NPD1/PD1)]. Identification and structural elucidation of these new families of bioactive mediators in resolution has opened the possibility of diverse pathophysiologic actions in several processes including infection, inflammatory pain, tissue regeneration, neuroprotection-neurodegenerative disorders, wound healing, and others.
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影响因子:
64.8
作者:
Chiang, Nan;Fredman, Gabrielle;Backhed, Fredrik;Oh, Sungwhan F.;Vickery, Thad;Schmidt, Birgitta A.;Serhan, Charles N.
通讯作者:
Serhan, Charles N.
DOI:
10.1073/pnas.0405445101
发表时间:
2004-10-19
影响因子:
11.1
作者:
Chiang, N;Bermudez, EA;Serhan, CN
通讯作者:
Serhan, CN
DOI:
10.1016/0006-291x(84)90601-6
发表时间:
1984-01-01
影响因子:
3.1
作者:
BAZAN, NG;BIRKLE, DL;REDDY, TS
通讯作者:
REDDY, TS
影响因子:
4.8
作者:
Chen, Ping;Vericel, Evelyne;Guichardant, Michel
通讯作者:
Guichardant, Michel
影响因子:
4.8
作者:
Biteman, Benjamin;Hassan, Iram R.;Gronert, Karsten
通讯作者:
Gronert, Karsten