PMID- 20977912
OWN - NLM
STAT- MEDLINE
DCOM- 20110510
LR  - 20171116
IS  - 1095-8584 (Electronic)
IS  - 0022-2828 (Linking)
VI  - 50
IP  - 1
DP  - 2011 Jan
TI  - Impact of long-term caloric restriction on cardiac senescence: caloric 
      restriction ameliorates cardiac diastolic dysfunction associated with aging.
PG  - 117-27
LID - 10.1016/j.yjmcc.2010.10.018 [doi]
AB  - Approximately half of older patients with congestive heart failure have normal 
      left ventricular (LV) systolic but abnormal LV diastolic function. In mammalian 
      hearts, aging is associated with LV diastolic dysfunction. Caloric restriction 
      (CR) is expected to retard cellular senescence and to attenuate the physiological 
      decline in organ function. Therefore, the aim of the present study was to 
      investigate the impact of long-term CR on cardiac senescence, in particular the 
      effect of CR on LV diastolic dysfunction associated with aging. Male 8-month-old 
      Fischer344 rats were divided into ad libitum fed and CR (40% energy reduction) 
      groups. LV function was evaluated by echocardiography and cardiac senescence was 
      compared between the two groups at the age of 30-month-old. (1) Echocardiography 
      showed similar LV systolic function, but better LV diastolic function in the CR 
      group. (2) Histological analysis revealed that CR attenuated the accumulation of 
      senescence-associated beta-galactosidase and lipofuscin and reduced myocyte 
      apoptosis. (3) In measurements of [Ca(2+)](i) transients, the time to 50% 
      relaxation was significantly smaller in the CR group, whereas F/F(0) was similar. 
      (4) CR attenuated the decrease in sarcoplasmic reticulum calcium ATPase 2 protein 
      with aging. (5) CR suppressed the mammalian target of rapamycin (mTOR) pathway 
      and increased the ratio of conjugated to cytosolic light chain 3, suggesting that 
      autophagy is enhanced in the CR hearts. In conclusion, CR improves diastolic 
      function in the senescent myocardium by amelioration of the age-associated 
      deterioration in intracellular Ca(2+) handling. Enhanced autophagy via the 
      suppression of mTOR during CR may retard cardiac senescence.
CI  - Copyright A(c) 2010 Elsevier Ltd. All rights reserved.
FAU - Shinmura, Ken
AU  - Shinmura K
AD  - Division of Geriatric Medicine, Department of Internal Medicine, Keio University 
      School of Medicine, Tokyo 160-8582, Japan. shimmura@sc.itc.keio.ac.jp
FAU - Tamaki, Kayoko
AU  - Tamaki K
FAU - Sano, Motoaki
AU  - Sano M
FAU - Murata, Mitsushige
AU  - Murata M
FAU - Yamakawa, Hiroyuki
AU  - Yamakawa H
FAU - Ishida, Hideyuki
AU  - Ishida H
FAU - Fukuda, Keiichi
AU  - Fukuda K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101023
PL  - England
TA  - J Mol Cell Cardiol
JT  - Journal of molecular and cellular cardiology
JID - 0262322
RN  - EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Aging/*physiology
MH  - Animals
MH  - Blotting, Western
MH  - Body Weight/physiology
MH  - Calcium/metabolism
MH  - *Caloric Restriction
MH  - Cellular Senescence/genetics/*physiology
MH  - Echocardiography
MH  - Male
MH  - Myocytes, Cardiac/cytology/*metabolism
MH  - Rats
MH  - Rats, Inbred F344
MH  - Sarcoplasmic Reticulum/metabolism
MH  - Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism
EDAT- 2010/10/28 06:00
MHDA- 2011/05/11 06:00
CRDT- 2010/10/28 06:00
PHST- 2010/06/02 00:00 [received]
PHST- 2010/10/05 00:00 [revised]
PHST- 2010/10/17 00:00 [accepted]
PHST- 2010/10/28 06:00 [entrez]
PHST- 2010/10/28 06:00 [pubmed]
PHST- 2011/05/11 06:00 [medline]
AID - S0022-2828(10)00397-4 [pii]
AID - 10.1016/j.yjmcc.2010.10.018 [doi]
PST - ppublish
SO  - J Mol Cell Cardiol. 2011 Jan;50(1):117-27. doi: 10.1016/j.yjmcc.2010.10.018. Epub 
      2010 Oct 23.