Regular ArticleRegional Energy Metabolism of Failing Hearts Following Myocardial Infarction
References (0)
Cited by (101)
Heat-shock protein 90 modulates cardiac ventricular hypertrophy via activation of MAPK pathway
2019, Journal of Molecular and Cellular CardiologyCitation Excerpt :The CM was separated by SDS-PAGE for western analysis of natriuretic peptide A (ANP). MI of rats was produced by ligation of the left ventricular (LV) coronary artery according to the method described previously [12]. Rats with myocardial infarction (coronary artery ligation (CAL) rats) and having an infarct area comprising approximately 40% of the left ventricle are consistently produced under our experimental conditions [13].
Effects of cardiosphere-derived cell transplantation on cardiac mitochondrial oxygen consumption after myocardial infarction in rats
2018, Biomedicine and PharmacotherapyCitation Excerpt :Heart failure represents the final common endpoint for various heart diseases, leading to cardiovascular death. In previous studies, we showed that decreased mitochondrial energy-producing ability in the remaining viable left ventricle was associated with the development of chronic heart failure following myocardial infarction in rats [1,2]. Therefore, it might be expected that preservation of mitochondrial function in the viable myocardium would play a key role in preventing the development of heart failure after a myocardial infarction.
Optimized CEST cardiovascular magnetic resonance for assessment of metabolic activity in the heart
2017, Journal of Cardiovascular Magnetic ResonanceMitochondrial function in heart failure: The impact of ischemic and non-ischemic etiology
2016, International Journal of CardiologyCitation Excerpt :In the human heart, 90% of ATP is produced by OXPHOS, therefore, an attenuation of this process in HF constitutes a major concern in terms of cardiac energy production [6,25,26]. Indeed, the current study confirms and extends previous work that has typically observed attenuated Complex I state 3 respiration in both animal models of HF and patients with HF [13,27,28]. Specifically, this study documents a HF-related attenuation in OXPHOS, per mg of tissue, assessed as Complex I, Complex II, and Complex I + II state 3 respiration, falling progressively from HdH to niHF, to iHF.
Protective effect of geranylgeranylacetone via enhanced induction of HSPB1 and HSPB8 in mitochondria of the failing heart following myocardial infarction in rats
2014, European Journal of PharmacologyCitation Excerpt :In our previous study, we showed that the contents of HSPB1 and HSPB8 were decreased in the mitochondrial fraction in the failing rat heart following myocardial infarction (Marunouchi et al., 2013). In the failing heart, the energy-producing ability of cardiac mitochondria is impaired (Sanbe et al., 1993). Although, those findings suggested that decreases in HSPB1 and HSPB8 contribute to the development of heart failure, roles of these heat shock proteins in the genesis and development of mitochondrial dysfunction in the failing heart remain unclear.
Possible involvement of HSP90-HSF1 multichaperone complex in impairment of HSP72 induction in the failing heart following myocardial infarction in rats
2013, Journal of Pharmacological Sciences