Formyl peptide receptor 2 as a potential therapeutic target for inflammatory bowel disease
© 2022. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society..
Inflammatory bowel disease (IBD) is a global health burden whose existing treatment is largely dependent on anti-inflammatory agents. Despite showing some therapeutic actions, their clinical efficacy and adverse events are unacceptable. Resolution as an active and orchestrated phase of inflammation involves improper inflammatory response with three key triggers, specialized pro-resolving mediators (SPMs), neutrophils and phagocyte efferocytosis. The formyl peptide receptor 2 (FPR2/ALX) is a human G protein-coupled receptor capable of binding SPMs and participates in the resolution process. This receptor has been implicated in several inflammatory diseases and its association with mouse model of IBD was established in some resolution-related studies. Here, we give an overview of three reported FPR2/ALX agonists highlighting their respective roles in pro-resolving strategies.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2023 |
---|---|
Erschienen: |
2023 |
Enthalten in: |
Zur Gesamtaufnahme - volume:44 |
---|---|
Enthalten in: |
Acta pharmacologica Sinica - 44(2023), 1 vom: 15. Jan., Seite 19-31 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Yang, Wen-Sheng [VerfasserIn] |
---|
Links: |
---|
Themen: |
Anti-Inflammatory Agents |
---|
Anmerkungen: |
Date Completed 06.01.2023 Date Revised 16.01.2023 published: Print-Electronic Citation Status MEDLINE |
---|
doi: |
10.1038/s41401-022-00944-0 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM343609053 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM343609053 | ||
003 | DE-627 | ||
005 | 20231226020839.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231226s2023 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1038/s41401-022-00944-0 |2 doi | |
028 | 5 | 2 | |a pubmed24n1145.xml |
035 | |a (DE-627)NLM343609053 | ||
035 | |a (NLM)35840658 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Yang, Wen-Sheng |e verfasserin |4 aut | |
245 | 1 | 0 | |a Formyl peptide receptor 2 as a potential therapeutic target for inflammatory bowel disease |
264 | 1 | |c 2023 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 06.01.2023 | ||
500 | |a Date Revised 16.01.2023 | ||
500 | |a published: Print-Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a © 2022. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society. | ||
520 | |a Inflammatory bowel disease (IBD) is a global health burden whose existing treatment is largely dependent on anti-inflammatory agents. Despite showing some therapeutic actions, their clinical efficacy and adverse events are unacceptable. Resolution as an active and orchestrated phase of inflammation involves improper inflammatory response with three key triggers, specialized pro-resolving mediators (SPMs), neutrophils and phagocyte efferocytosis. The formyl peptide receptor 2 (FPR2/ALX) is a human G protein-coupled receptor capable of binding SPMs and participates in the resolution process. This receptor has been implicated in several inflammatory diseases and its association with mouse model of IBD was established in some resolution-related studies. Here, we give an overview of three reported FPR2/ALX agonists highlighting their respective roles in pro-resolving strategies | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Review | |
650 | 4 | |a FPR2/ALX | |
650 | 4 | |a IBD | |
650 | 4 | |a SPM | |
650 | 4 | |a inflammation | |
650 | 4 | |a pro-resolving | |
650 | 4 | |a resolution | |
650 | 7 | |a Receptors, Formyl Peptide |2 NLM | |
650 | 7 | |a Anti-Inflammatory Agents |2 NLM | |
700 | 1 | |a Wang, Jing-Lin |e verfasserin |4 aut | |
700 | 1 | |a Wu, Wei |e verfasserin |4 aut | |
700 | 1 | |a Wang, Guang-Fei |e verfasserin |4 aut | |
700 | 1 | |a Yan, Jun |e verfasserin |4 aut | |
700 | 1 | |a Liu, Qing |e verfasserin |4 aut | |
700 | 1 | |a Wu, Xiao-Yan |e verfasserin |4 aut | |
700 | 1 | |a Zhou, Qing-Tong |e verfasserin |4 aut | |
700 | 1 | |a Yang, De-Hua |e verfasserin |4 aut | |
700 | 1 | |a Wang, Ming-Wei |e verfasserin |4 aut | |
700 | 1 | |a Li, Zhi-Ping |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Acta pharmacologica Sinica |d 2000 |g 44(2023), 1 vom: 15. Jan., Seite 19-31 |w (DE-627)NLM111735181 |x 1745-7254 |7 nnns |
773 | 1 | 8 | |g volume:44 |g year:2023 |g number:1 |g day:15 |g month:01 |g pages:19-31 |
856 | 4 | 0 | |u http://dx.doi.org/10.1038/s41401-022-00944-0 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 44 |j 2023 |e 1 |b 15 |c 01 |h 19-31 |