High-fat diet-induced juvenile obesity leads to cardiomyocyte dysfunction and upregulation of Foxo3a transcription factor independent of lipotoxicity and apoptosis

Relling, David P.; Esberg, Lucy B.; Fang, Cindy X.; Johnson, W. Thomas; Murphy, Eric J.; Carlson, Edward C.; Saari, Jack T.; Ren, Jun

doi:10.1097/01.hjh.0000203846.34314.94

Cited by 134 publications

(210 citation statements)

References 56 publications

(113 reference statements)

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“…Blood pressure is controlled via several systems, among them the sympathetic nervous system, reninangiotensin aldosterone system, and oxidative stress, which causes peripheral vasoconstriction [26][27][28] . This hypertension observed in rats subjected to stress is probably related to systems mentioned above; however, these mechanisms were not assessed in this particular study.…”

Section: Discussionmentioning

confidence: 99%

Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Bruder‐Nascimento

Campos

Leopoldo

et al. 2012

Arq. Bras. Cardiol.

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Section: Discussionmentioning

confidence: 99%

Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Bruder‐Nascimento

Campos

Leopoldo

et al. 2012

Arq. Bras. Cardiol.

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“…The Aconitase-340 assayÔ measures NADPH formation, a product of the oxidation of isocitrate to aketoglutarate. Tris-HCl buffer (pH 7.4) was served as blank (37).…”

Section: Aconitase Activitymentioning

confidence: 99%

Retracted: Activation of Akt Rescues Endoplasmic Reticulum Stress-Impaired Murine Cardiac Contractile Function via Glycogen Synthase Kinase-3β-Mediated Suppression of Mitochondrial Permeation Pore Opening

Zhang

Zhi

Cour

et al. 2011

Antioxidants & Redox Signaling

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Aims: The present study was designed to examine the impact of chronic Akt activation on endoplasmic reticulum (ER) stress-induced cardiac mechanical anomalies, if any, and the underlying mechanism involved. Results: Wild-type and transgenic mice with cardiac-specific overexpression of the active mutant of Akt (Myr-Akt) were subjected to the ER stress inducer tunicamycin (1 or 3 mg/kg). ER stress led to compromised echocardiographic (elevated left ventricular end-systolic diameter and reduced fractional shortening) and cardiomyocyte contractile function, intracellular Ca 2+ mishandling, and cell survival in wild-type mice associated with mitochondrial damage. In vitro ER stress induction in murine cardiomyocytes upregulated the ER stress proteins Gadd153, GRP78, and phospho-eIF2a, and promoted reactive oxygen species production, carbonyl formation, apoptosis, mitochondrial membrane potential loss, and mitochondrial permeation pore (mPTP) opening associated with overtly impaired cardiomyocyte contractile and intracellular Ca 2+ properties. Interestingly, these anomalies were mitigated by chronic Akt activation or the ER chaperon tauroursodeoxycholic acid (TUDCA). Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3b (GSK3b) (leading to activation of GSK3b), the effect of which was abrogated by Akt activation and TUDCA. The ER stress-induced cardiomyocyte contractile and mitochondrial anomalies were obliterated by the mPTP inhibitor cyclosporin A, GSK3b inhibitor SB216763, and ER stress inhibitor TUDCA. Innovation: This research reported the direct relationship between ER stress and cardiomyocyte contractile and mitochondrial anomalies for the first time. Conclusion: Taken together, these data suggest that ER stress may compromise cardiac contractile and intracellular Ca 2+ properties, possibly through the Akt/GSK3b-dependent impairment of mitochondrial integrity. Antioxid. Redox Signal. 15, 2407-2424.

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“…In addition, the obese rats developed metabolic disorders such as glucose intolerance, hyperinsulinemia and hyperleptinemia, characteristics commonly related to human obesity 15,19,20 . Insulin-resistance, defined as decreased sensitivity and/or responsiveness to metabolic actions of insulin, is a cardinal feature of diabetes, obesity and dyslipidemia 21 .…”

Section: Time (Min)mentioning

confidence: 99%

Alterações vasculares em ratos obesos por dieta rica em gordura: papel da Via L-arginina/NO Endotelial

Nascimento¹,

Baptista²,

Pereira³

et al. 2011

Arq. Bras. Cardiol.

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High-fat diet-induced juvenile obesity leads to cardiomyocyte dysfunction and upregulation of Foxo3a transcription factor independent of lipotoxicity and apoptosis

Abstract: Collectively, our data show that high-fat diet-induced obesity resulted in impaired cardiomyocyte function, upregulated Foxo3a transcription factor and mitochondrial damage without overt lipotoxicity or apoptosis.

Cited by 134 publications

References 56 publications

Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Estresse crônico melhora a função miocárdica sem alterar a atividade do canal-L para Ca+2 em ratos

Retracted: Activation of Akt Rescues Endoplasmic Reticulum Stress-Impaired Murine Cardiac Contractile Function via Glycogen Synthase Kinase-3β-Mediated Suppression of Mitochondrial Permeation Pore Opening

Alterações vasculares em ratos obesos por dieta rica em gordura: papel da Via L-arginina/NO Endotelial

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