2024-03-28T18:34:09Z
https://nagoya.repo.nii.ac.jp/oai
oai:nagoya.repo.nii.ac.jp:00017399
2023-11-16T05:32:03Z
499:508:509:1563
Premature Cardiac Senescence in DahlS.Z-Lepr fa/Lepr fa Rats as a New Animal Model of Metabolic Syndrome
TAKAHASHI, KEIJI
51109
TAKATSU, MIWA
51110
HATTORI, TAKUYA
51111
MURASE, TAMAYO
51112
OHURA, SAE
51113
TAKESHITA, YUURI
51114
WATANABE, SHOGO
51115
MUROHARA, TOYOAKI
51116
NAGATA, KOHZO
51117
metabolic syndrome
cardiac remodeling
oxidative stress
renin-angiotensin-aldosterone system
cardiac senescence
2014-02
Aging is accelerated by metabolic and cardiovascular diseases, and the risk of these diseases increases with age. Obesity is an important risk factor for many age-related diseases and is linked to reduced telomere length in white blood cells. We investigated whether cardiac senescence might be enhanced in DahlS.ZLepr fa/Lepr fa (DS/obese) rats, which we recently established as a new animal model of metabolic syndrome. The heart of DS/obese rats was compared with that of homozygous lean littermates (DahlS.Z-Lepr+/Lepr+, or DS/lean, rats). DS/obese rats manifested hypertension as well as left ventricular hypertrophy, fibrosis, and diastolic dysfunction at 18 weeks of age. Myocardial oxidative stress and inflammation were increased in DS/obese rats compared with DS/lean rats. Telomere length in myocardial cells did not differ between the two rat strains, whereas telomerase activity and expression of the telomerase reverse transcriptase gene were increased in DS/obese rats. Expression of the senescence-associated genes for checkpoint kinase 2 (Chk2), p53, and p21 as well as that of genes related to the renin-angiotensin-aldosterone system were also up-regulated in the DS/obese rat heart. Our results indicate that DS/obese rats undergo premature cardiac senescence as well as cardiac remodeling in association with the development of diastolic dysfunction in these animals.
departmental bulletin paper
Nagoya University School of Medicine
2014-02
Nagoya Journal of Medical Science
1-2
76
35
49
http://hdl.handle.net/2237/19482
2186-3326
0027-7622
eng
http://www.med.nagoya-u.ac.jp/medlib/nagoya_j_med_sci/7612/7612.html