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Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
West Ashley Library
9 a.m. - 4 p.m.
Phone: (843) 766-6635
Wando Mount Pleasant Library
9 a.m. - 6 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. - 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. - 6 p.m.
Phone: (843) 889-3300
Otranto Road Library
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McClellanville Library
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Keith Summey North Charleston Library
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John's Island Library
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Hurd/St. Andrews Library
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Phone: (843) 795-6679
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Phone: (843) 805-6930
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Phone: (843) 805-6909
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Ablation of cardiac TIGAR preserves myocardial energetics and cardiac function in the pressure overload heart failure model.
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- Author(s): Yoshifumi Okawa; Atsushi Hoshino; Makoto Ariyoshi; Satoshi Kaimoto; Shuhei Tateishi; Kazunori Ono; Motoki Uchihashi; Iwai-Kanai, Eri; Satoaki Matoba
- Source:
American Journal of Physiology: Heart & Circulatory Physiology; Jun2019, Vol. 316 Issue 6, pH1366-H1377, 12p- Subject Terms:
- Source:
- Additional Information
- Abstract: Despite the advances in medical therapy, the morbidity and mortality of heart failure (HF) remain unacceptably high. HF results from reduced metabolism- contraction coupling efficiency, so the modulation of cardiac metabolism may be an effective strategy for therapeutic interventions. Tumor suppressor p53 (TP53) and its downstream target TP53-induced glycolysis and apoptosis regulator (TIGAR) are known to modulate cardiac metabolism and cell fate. To investigate TIGAR's function in HF, we compared myocardial, metabolic, and functional outcomes between TIGAR knockout (TIGAR-/-) mice and wild-type (TIGAR+/+) mice subjected to chronic thoracic transverse aortic constriction (TAC), a pressure-overload HF model. In wild-type mice hearts, p53 and TIGAR increased markedly during HF development. Eight weeks after TAC surgery, the left ventricular (LV) dysfunction, fibrosis, oxidative damage, and myocyte apoptosis were significantly advanced in wild-type than in TIGAR-/- mouse heart. Further, myocardial high-energy phosphates in wild-type hearts were significantly decreased compared with those of TIGAR-/- mouse heart. Glucose oxidation and glycolysis rates were also reduced in isolated perfused wild-type hearts following TAC than those in TIGAR-/- hearts, which suggest that the upregulation of TIGAR in HF causes impaired myocardial energetics and function. The effects of TIGAR knockout on LV function were also replicated in tamoxifen (TAM)-inducible cardiac-specific TIGAR knockout mice (TIGARflox/flox/Tg(Myh6-cre/ Esr1) mice). The ablation of TIGAR during pressure-overload HF preserves myocardial function and energetics. Thus, cardiac TIGARtargeted therapy to increase glucose metabolism will be a novel strategy for HF. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of American Journal of Physiology: Heart & Circulatory Physiology is the property of American Physiological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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