PMID- 21921294
OWN - NLM
STAT- MEDLINE
DCOM- 20120111
LR  - 20161125
IS  - 1552-4531 (Electronic)
IS  - 0748-7304 (Linking)
VI  - 26
IP  - 5
DP  - 2011 Oct
TI  - The circadian clock influences heart performance.
PG  - 402-11
LID - 10.1177/0748730411414168 [doi]
AB  - Circadian clocks are believed to provide the selective advantage of anticipation, 
      thus allowing organisms to respond efficiently to stimuli at the appropriate 
      moment. Disrupted circadian rhythms have been found to affect a variety of basic 
      physiological processes. However, the importance of the circadian clock in 
      regulating heart performance remains undetermined. We hypothesized that the 
      circadian clock plays a crucial role in heart performance through the 
      anticipation of daily workload. Echocardiography was employed to monitor heart 
      function and structure in mice in a noninvasive, real-time manner. In wild-type 
      mice, both the ejection fraction (EF) and the shortening fraction (FS), two 
      important markers of cardiac function, show diurnal variation. In addition, the 
      amplitude of the EF and the FS enlarges in response to forced exercise in a 
      time-dependent manner. The diurnal variations in EF and FS are altered in mice 
      with disruptions in circadian clock genes and are significantly attenuated under 
      an imposed light regimen. Furthermore, it shows that the overexpression of 
      peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Pgc1alpha) 
      under control of the muscle creatine kinase (MCK) promoter inhibited clock gene 
      expression in the heart and muscle and decreased the expression of peroxisome 
      proliferator-activated receptor alpha (Pparalpha), metabolic genes glucose 
      transporter (Glut4), and acetyl-coA synthetase (Acs1). Pgc1alpha overexpression 
      abolished the diurnal variation of EF. We thus propose that PGC1alpha might play an 
      important role in circadian-mediated, impaired cardiac function by regulating the 
      circadian rhythm of metabolic genes.
CI  - (c) 2011 The Author(s)
FAU - Wu, Xi
AU  - Wu X
AD  - MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research 
      Center, Nanjing University, Nanjing, China.
FAU - Liu, Zhiwei
AU  - Liu Z
FAU - Shi, Guangsen
AU  - Shi G
FAU - Xing, Lijuan
AU  - Xing L
FAU - Wang, Xiaohan
AU  - Wang X
FAU - Gu, Xiwen
AU  - Gu X
FAU - Qu, Zhipeng
AU  - Qu Z
FAU - Dong, Zhen
AU  - Dong Z
FAU - Xiong, Jing
AU  - Xiong J
FAU - Gao, Xiang
AU  - Gao X
FAU - Zhang, Chenyu
AU  - Zhang C
FAU - Xu, Ying
AU  - Xu Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Biol Rhythms
JT  - Journal of biological rhythms
JID - 8700115
RN  - 0 (Glucose Transporter Type 4)
RN  - 0 (PPAR alpha)
RN  - 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
RN  - 0 (Ppargc1a protein, mouse)
RN  - 0 (Slc2a4 protein, mouse)
RN  - 0 (Trans-Activators)
RN  - 0 (Transcription Factors)
RN  - EC 2.3.1.48 (CLOCK Proteins)
RN  - EC 2.7.3.2 (Creatine Kinase, MM Form)
RN  - EC 6.2.1.- (Coenzyme A Ligases)
RN  - EC 6.2.1.13 (acetate-CoA ligase (ADP-forming))
SB  - IM
MH  - Animals
MH  - CLOCK Proteins
MH  - Circadian Clocks/*physiology
MH  - Coenzyme A Ligases/biosynthesis
MH  - Creatine Kinase, MM Form/genetics
MH  - Echocardiography
MH  - Glucose Transporter Type 4/biosynthesis
MH  - Heart/*physiology
MH  - Mice
MH  - Mice, Transgenic
MH  - Motor Activity
MH  - PPAR alpha/biosynthesis/genetics
MH  - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
MH  - Promoter Regions, Genetic/physiology
MH  - Trans-Activators/*biosynthesis/genetics
MH  - Transcription Factors
EDAT- 2011/09/17 06:00
MHDA- 2012/01/12 06:00
CRDT- 2011/09/17 06:00
PHST- 2011/09/17 06:00 [entrez]
PHST- 2011/09/17 06:00 [pubmed]
PHST- 2012/01/12 06:00 [medline]
AID - 26/5/402 [pii]
AID - 10.1177/0748730411414168 [doi]
PST - ppublish
SO  - J Biol Rhythms. 2011 Oct;26(5):402-11. doi: 10.1177/0748730411414168.