Lecarpentier Yves, Claes Victor, Duthoit Guillaume, Hébert Jean-Louis
Centre de Recherche Clinique, Centre Hospitalier Régional de Meaux Meaux, France.
Department of Pharmaceutical Sciences, University of Antwerp Wilrijk, Belgium.
Front Physiol. 2014 Nov 4;5:429. doi: 10.3389/fphys.2014.00429. eCollection 2014.
Circadian clock mechanisms are far-from-equilibrium dissipative structures. Peroxisome proliferator-activated receptors (PPAR alpha, beta/delta, and gamma) play a key role in metabolic regulatory processes, particularly in heart muscle. Links between circadian rhythms (CRs) and PPARs have been established. Mammalian CRs involve at least two critical transcription factors, CLOCK and BMAL1 (Gekakis et al., 1998; Hogenesch et al., 1998). PPAR gamma plays a major role in both glucose and lipid metabolisms and presents circadian properties which coordinate the interplay between metabolism and CRs. PPAR gamma is a major component of the vascular clock. Vascular PPAR gamma is a peripheral regulator of cardiovascular rhythms controlling circadian variations in blood pressure and heart rate through BMAL1. We focused our review on diseases with abnormalities of CRs and with primary or secondary cardiac dysfunction. Moreover, these diseases presented changes in the Wnt/beta-catenin pathway and PPARs, according to two opposed profiles. Profile 1 was defined as follows: inactivation of the Wnt/beta-catenin pathway with increased expression of PPAR gamma. Profile 2 was defined as follows: activation of the Wnt/beta-catenin pathway with decreased expression of PPAR gamma. A typical profile 1 disease is arrhythmogenic right ventricular cardiomyopathy, a genetic cardiac disease which presents mutations of the desmosomal proteins and is mainly characterized by fatty acid accumulation in adult cardiomyocytes mainly in the right ventricle. The link between PPAR gamma dysfunction and desmosomal genetic mutations occurs via inactivation of the Wnt/beta-catenin pathway presenting oscillatory properties. A typical profile 2 disease is type 2 diabetes, with activation of the Wnt/beta-catenin pathway and decreased expression of PPAR gamma. CRs abnormalities are present in numerous pathologies such as cardiovascular diseases, sympathetic/parasympathetic dysfunction, hypertension, diabetes, neurodegenerative diseases, cancer which are often closely inter-related.
昼夜节律时钟机制是远离平衡的耗散结构。过氧化物酶体增殖物激活受体(PPARα、β/δ和γ)在代谢调节过程中起关键作用,尤其是在心肌中。昼夜节律(CRs)与PPARs之间的联系已经建立。哺乳动物的CRs涉及至少两个关键转录因子,即CLOCK和BMAL1(Gekakis等人,1998年;Hogenesch等人,1998年)。PPARγ在葡萄糖和脂质代谢中都起主要作用,并具有昼夜节律特性,可协调代谢与CRs之间的相互作用。PPARγ是血管时钟的主要组成部分。血管PPARγ是心血管节律的外周调节因子,通过BMAL1控制血压和心率的昼夜变化。我们的综述聚焦于CRs异常以及原发性或继发性心脏功能障碍的疾病。此外,根据两种相反的模式,这些疾病在Wnt/β-连环蛋白通路和PPARs方面呈现出变化。模式1定义如下:Wnt/β-连环蛋白通路失活,PPARγ表达增加。模式2定义如下:Wnt/β-连环蛋白通路激活,PPARγ表达降低。一种典型的模式1疾病是致心律失常性右室心肌病,这是一种遗传性心脏病,表现为桥粒蛋白突变,主要特征是成年心肌细胞尤其是右心室中脂肪酸积聚。PPARγ功能障碍与桥粒基因突变之间的联系是通过呈现振荡特性的Wnt/β-连环蛋白通路失活而发生的。一种典型的模式2疾病是2型糖尿病,其Wnt/β-连环蛋白通路激活,PPARγ表达降低。CRs异常存在于许多疾病中,如心血管疾病、交感/副交感神经功能障碍、高血压、糖尿病、神经退行性疾病、癌症,这些疾病往往密切相关。