Molecular regulation of brain metabolism underlying circadian epilepsy.
Molecular regulation of brain metabolism underlying circadian epilepsy.
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作者：
Chan F;Liu J
广泛的研究表明，癫痫在24小时周期中的某些时间段以更高的频率发生。尽管这些发现暗示了昼夜节律和癫痫之间的重叠，但这种昼夜节律背后的分子和细胞机制尚不清楚。因为24小时节律是由昼夜节律分子系统产生的，所以这个由许多昼夜节律基因组成的系统与癫痫有关也就不足为奇了。我们总结了文献中涉及多种昼夜节律基因的证据，如CLOCK、BMAL1、PER1、REV-ERBα和RORα与癫痫有关。在癫痫的各种动物模型中，这些基因的昼夜振荡和稳态水平被打乱。这些基因的下游途径涉及与癫痫相关的大量代谢途径。这些途径包括吡哆醇代谢，雷帕霉素途径的哺乳动物靶点，以及氧化还原状态的调节。我们认为，这些代谢途径的破坏可能参与癫痫的昼夜节律调节。更好地理解癫痫昼夜节律的细胞和分子机制，将使我们能够准确地针对癫痫的昼夜节律紊乱，寻找一种新的治疗方法。
Extensive study has demonstrated that epilepsy occurs with greater frequency at certain times in the 24-h cycle. Although these findings implicate an overlap between the circadian rhythm and epilepsy, the molecular and cellular mechanisms underlying this circadian regulation are poorly understood. Because the 24-h rhythm is generated by the circadian molecular system, it is not surprising that this system comprised of many circadian genes is implicated in epilepsy. We summarized evidence in the literature implicating various circadian genes such as Clock, Bmal1, Per1, Rev-erbα, and Rorα in epilepsy. In various animal models of epilepsy, the circadian oscillation and the steady-state level of these genes are disrupted. The downstream pathway of these genes involves a large number of metabolic pathways associated with epilepsy. These pathways include pyridoxal metabolism, the mammalian target of rapamycin pathway, and the regulation of redox state. We propose that disruption of these metabolic pathways could mediate the circadian regulation of epilepsy. A greater understanding of the cellular and molecular mechanism of circadian regulation of epilepsy would enable us to precisely target the circadian disruption in epilepsy for a novel therapeutic approach.
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影响因子：
29
作者：
Chaix A;Lin T;Le HD;Chang MW;Panda S
通讯作者：
Panda S
DOI：
10.1038/s41436-018-0060-2
发表时间：
2019-03
期刊：
Genetics in medicine : official journal of the American College of Medical Genetics
影响因子：
--
作者：
Baldassari S;Picard F;Verbeek NE;van Kempen M;Brilstra EH;Lesca G;Conti V;Guerrini R;Bisulli F;Licchetta L;Pippucci T;Tinuper P;Hirsch E;de Saint Martin A;Chelly J;Rudolf G;Chipaux M;Ferrand-Sorbets S;Dorfmüller G;Sisodiya S;Balestrini S;Schoeler N;Hernandez-Hernandez L;Krithika S;Oegema R;Hagebeuk E;Gunning B;Deckers C;Berghuis B;Wegner I;Niks E;Jansen FE;Braun K;de Jong D;Rubboli G;Talvik I;Sander V;Uldall P;Jacquemont ML;Nava C;Leguern E;Julia S;Gambardella A;d'Orsi G;Crichiutti G;Faivre L;Darmency V;Benova B;Krsek P;Biraben A;Lebre AS;Jennesson M;Sattar S;Marchal C;Nordli DR Jr;Lindstrom K;Striano P;Lomax LB;Kiss C;Bartolomei F;Lepine AF;Schoonjans AS;Stouffs K;Jansen A;Panagiotakaki E;Ricard-Mousnier B;Thevenon J;de Bellescize J;Catenoix H;Dorn T;Zenker M;Müller-Schlüter K;Brandt C;Krey I;Polster T;Wolff M;Balci M;Rostasy K;Achaz G;Zacher P;Becher T;Cloppenborg T;Yuskaitis CJ;Weckhuysen S;Poduri A;Lemke JR;Møller RS;Baulac S
通讯作者：
Baulac S
影响因子：
3.7
作者：
de Vries PJ;Belousova E;Benedik MP;Carter T;Cottin V;Curatolo P;Dahlin M;D'Amato L;d'Augères GB;Ferreira JC;Feucht M;Fladrowski C;Hertzberg C;Jozwiak S;Kingswood JC;Lawson JA;Macaya A;Marques R;Nabbout R;O'Callaghan F;Qin J;Sander V;Sauter M;Shah S;Takahashi Y;Touraine R;Youroukos S;Zonnenberg B;Jansen AC;TOSCA Consortium and TOSCA Investigators
通讯作者：
TOSCA Consortium and TOSCA Investigators
影响因子：
8
作者：
Chen, Zheng;Yoo, Seung-Hee;Takahashi, Joseph S.
通讯作者：
Takahashi, Joseph S.
影响因子：
--
作者：
Ben-Cherif, Wafa;Dridi, Ichrak;Boughattas, Naceur A
通讯作者：
Boughattas, Naceur A