{"title":"溶血磷脂酰胆碱16:0:重度纤维肌痛的有希望的生物标志物","authors":"A. Delage","doi":"10.3166/dea-2021-0169","DOIUrl":null,"url":null,"abstract":"Fibromyalgia (FM) is a complex disease without any clear physiopathology, thus treating FM remains challenging for physicians. In this article Hung et al. propose a new mouse model of FM in which adult mice are exposed to repeated and intermittent sound stress (RISS). These stressors are shown to have an effect at the cellular level: leucocytes generate a high amount of reactive oxygen species (ROS), which triggers plasma lipid peroxidation and an excessive production of lysophosphatidylcholine (LPC) 16:0. LPC16:0 molecules then activate acid-sensing ion channel 3 (ASIC3) on muscle nociceptors, generating a central sensitization process responsible for the development of FM-like phenotypes (hyperalgesia, chronic fatigue, and anxiety). In the second part, a clinical investigation was performed on patients suffering from mild and severe FM. During the month preceding the study, FM patients perceived more daily stressors than healthy controls (HC). In severe FM patients, LPC16:0 levels are correlated with ongoing pain severity. This study suggests that LPC16:0 could be a biomarker for FM, particularly in its severe forms, and proposes to further investigate the effects of platelet-activating factor acetylhydrolase (PAF-AH) inhibitors such as darapladib on fibromyalgia. These molecules could prove to be interesting therapeutic compounds for the treatment of severe FM.","PeriodicalId":11303,"journal":{"name":"Douleur Et Analgesie","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Lysophosphatidylcholine 16:0, a Promising Biomarker for Severe Fibromyalgia\",\"authors\":\"A. Delage\",\"doi\":\"10.3166/dea-2021-0169\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Fibromyalgia (FM) is a complex disease without any clear physiopathology, thus treating FM remains challenging for physicians. In this article Hung et al. propose a new mouse model of FM in which adult mice are exposed to repeated and intermittent sound stress (RISS). These stressors are shown to have an effect at the cellular level: leucocytes generate a high amount of reactive oxygen species (ROS), which triggers plasma lipid peroxidation and an excessive production of lysophosphatidylcholine (LPC) 16:0. LPC16:0 molecules then activate acid-sensing ion channel 3 (ASIC3) on muscle nociceptors, generating a central sensitization process responsible for the development of FM-like phenotypes (hyperalgesia, chronic fatigue, and anxiety). In the second part, a clinical investigation was performed on patients suffering from mild and severe FM. During the month preceding the study, FM patients perceived more daily stressors than healthy controls (HC). In severe FM patients, LPC16:0 levels are correlated with ongoing pain severity. This study suggests that LPC16:0 could be a biomarker for FM, particularly in its severe forms, and proposes to further investigate the effects of platelet-activating factor acetylhydrolase (PAF-AH) inhibitors such as darapladib on fibromyalgia. These molecules could prove to be interesting therapeutic compounds for the treatment of severe FM.\",\"PeriodicalId\":11303,\"journal\":{\"name\":\"Douleur Et Analgesie\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Douleur Et Analgesie\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3166/dea-2021-0169\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Douleur Et Analgesie","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3166/dea-2021-0169","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
Lysophosphatidylcholine 16:0, a Promising Biomarker for Severe Fibromyalgia
Fibromyalgia (FM) is a complex disease without any clear physiopathology, thus treating FM remains challenging for physicians. In this article Hung et al. propose a new mouse model of FM in which adult mice are exposed to repeated and intermittent sound stress (RISS). These stressors are shown to have an effect at the cellular level: leucocytes generate a high amount of reactive oxygen species (ROS), which triggers plasma lipid peroxidation and an excessive production of lysophosphatidylcholine (LPC) 16:0. LPC16:0 molecules then activate acid-sensing ion channel 3 (ASIC3) on muscle nociceptors, generating a central sensitization process responsible for the development of FM-like phenotypes (hyperalgesia, chronic fatigue, and anxiety). In the second part, a clinical investigation was performed on patients suffering from mild and severe FM. During the month preceding the study, FM patients perceived more daily stressors than healthy controls (HC). In severe FM patients, LPC16:0 levels are correlated with ongoing pain severity. This study suggests that LPC16:0 could be a biomarker for FM, particularly in its severe forms, and proposes to further investigate the effects of platelet-activating factor acetylhydrolase (PAF-AH) inhibitors such as darapladib on fibromyalgia. These molecules could prove to be interesting therapeutic compounds for the treatment of severe FM.
期刊介绍:
Douleur et Analgésie, première revue internationale francophone consacrée à la douleur, a été créée en 1988. De par la qualité scientifique et l’indépendance de ses publications, ce trimestriel a reçu d’emblée un accueil favorable auprès des chercheurs et cliniciens spécialisés dans le domaine. Á l’occasion de la reprise de la revue en 2006 par les Éditions Springer, le comité éditorial a souhaité s’ouvrir davantage à la francophonie, y compris nord américaine, pour mieux partager les connaissances et renforcer la valeur scientifique de la revue.