RETRACTED: Angiotensin receptor blockade improves the net balance of cardiac Ca2+ handling-related proteins in sympathetic hyperactivity-induced heart failure

Ferreira, Julio Cesar Batista; Moreira, José Bianco Nascimento; Campos, Juliane C.; Pereira, Maria Alice Ornellas; Mattos, Katt Coelho; Coelho, Marcele A.; Brum, Patrícia Chakur

doi:10.1016/j.lfs.2011.01.009

Cited by 22 publications

(20 citation statements)

References 39 publications

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“…However, Losartan also induced an increase on cardiac SERCA2a gene expression. This observation is in agreement with a previous study, which demonstrated that the blockade of AT1R promoted an increase on cardiac SERCA2a levels [18].…”

Section: Discussionsupporting

confidence: 94%

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

et al. 2015

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Elevated thyroid hormone (TH) levels induce cardiac hypertrophy partially via type 1 Angiotensin II receptor (AT1R). MicroRNAs (miRNAs) are key regulators of cardiac homeostasis, and miR-133 has been shown to be involved in cardiac hypertrophy. However, the potential role of miR-133 in cardiac growth induced by TH is unknown. Thus, we aimed to investigate the miR-133 expression, as well as its potential role in cardiac hypertrophy in response to TH. Wistar rats were subjected to hyperthyroidism combined or not with the AT1R blocker. T3 serum levels were assessed to confirm the hyperthyroid status. TH induced cardiac hypertrophy, as evidenced by higher cardiac weight/tibia length ratio and α-actin mRNA levels, which was prevented by AT1R blocker. miR-133 expression was decreased in TH-induced cardiac hypertrophy in part through the AT1R. Additionally, the cardiac mRNA levels of miR-133 targets, SERCA2a and calcineurin were increased in hyperthyroidism partially via AT1R, as evaluated by real-time RT-PCR. Interestingly, miR-133 levels were unchanged in T3-induced cardiomyocyte hypertrophy in vitro. However, a gain-of-function study revealed that miR-133 mimic blunted the T3-induced cardiomyocyte hypertrophy in vitro. Together, our data indicate that miR-133 expression is reduced in TH-induced cardiac hypertrophy partially by the AT1R and that miR-133 mimic prevents the cardiomyocyte hypertrophy in response to T3 in vitro. These findings provide new insights regarding the mechanisms involved in the cardiac growth mediated by TH, suggesting that miR-133 plays a key role in TH-induced cardiomyocyte hypertrophy.

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Section: Discussionsupporting

confidence: 94%

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

et al. 2015

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“…The change in the caffeine-induced Ca 2+ release curve was potentially due to Losartan increasing the expression of NCX [32], which is the sole channel responsible for clearing Ca 2+ from the cytosol during treatment with caffeine. It is, however, unlikely that Ca 2+ signaling is the entire mechanism of improvement following Losartan treatment as tumor-induced changes in the amplitude of the Ca 2+ transient are unaffected by Losartan.…”

Section: Discussionmentioning

confidence: 99%

Losartan treatment attenuates tumor-induced myocardial dysfunction

Stevens

Velten²,

Youtz

et al. 2015

Journal of Molecular and Cellular Cardiology

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Fatigue and muscle wasting are common symptoms experienced by cancer patients. Data from animal models demonstrate that angiotensin is involved in tumor-induced muscle wasting, and that tumor growth can independently affect myocardial function, which could contribute to fatigue in cancer patients. In clinical studies, inhibitors of angiotensin converting enzyme (ACE) can prevent the development of chemotherapy-induced cardiovascular dysfunction, suggesting a mechanistic role for the renin-angiotensin-aldosterone system (RAAS). In the present study, we investigated whether an angiotensin (AT)1-receptor antagonist could prevent the development of tumor-associated myocardial dysfunction. Methods and Results: Colon26 adenocarcinoma (c26) cells were implanted into female CD2F1 mice at 8 weeks of age. Simultaneously, mice were administered Losartan (10 mg/kg) daily via their drinking water. In vivo echocardiography, blood pressure, in vitro cardiomyocyte function, cell proliferation assays, and measures of systemic inflammation and myocardial protein degradation were performed 19 days following tumor cell injection. Losartan treatment prevented tumor-induced loss of muscle mass and in vitro c26 cell proliferation, decreased tumor weight, and attenuated myocardial expression of interleukin-6. Furthermore, Losartan treatment mitigated tumor-associated alterations in calcium signaling in cardiomyocytes, which was associated with improved myocyte contraction velocity, systolic function, and blood pressures in the hearts of tumor-bearing mice. Conclusions: These data suggest that Losartan may mitigate tumor-induced myocardial dysfunction and inflammation.

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“…Other angiotensin II related drugs, losartan (an ARB) and temocapril (an inhibitor of angiotensin converting enzyme), have been shown to have protective effects against both the abnormal amounts of PLB and SERCA and the LV dysfunction associated with sympathetic hyperactivityinduced heart failure and salt-induced hypertension (Satoh et al 2003;Ferreira et al 2011). Telmisartan has been previously shown (D) CF rate (CFR) was calculated by dividing CF by heart mass.…”

Section: Discussionmentioning

confidence: 99%

Abnormal amounts of intracellular calcium regulatory proteins in SHRSP.Z-Lepr^fa/IzmDmcr rats with metabolic syndrome and cardiac dysfunction

Kagota

Maruyama

Tada

et al. 2013

Can. J. Physiol. Pharmacol.

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Metabolic syndrome is known to increase the risk of abnormal cardiac structure and function, which are considered to contribute to increased incidence of cardiovascular disease and mortality. We previously demonstrated that ventricular hypertrophy and diastolic dysfunction occur in SHRSP.Z-Lepr(fa)/IzmDmcr (SHRSP fatty) rats with metabolic syndrome. The aim of this study was to investigate the possible mechanisms underlying abnormal heart function in SHRSP fatty rats. The amount of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) 2a, phospholamban (PLB) protein, and Ser(16)-phosphorylated PLB was decreased in cardiomyocytes from SHRSP fatty rats compared with those from control Wistar-Kyoto rats at 18 weeks of age, and the PLB-to-SERCA2a ratio was increased. Left ventricular developed pressure was unchanged, and coronary flow rate and maximum rate of left ventricular pressure decline (-dP/dt) was decreased in SHRSP fatty rats. Treatment with telmisartan reversed the abnormalities of PLB amount, coronary flow rate, and -dP/dt in SHRSP fatty rats. These results indicate that abnormal amounts of intracellular Ca(2+) regulatory proteins in cardiomyocytes, leading to reduced intracellular Ca(2+) reuptake into the sarcoplasmic reticulum, may play a role in the diastolic dysfunction in SHRSP fatty rats and that these effects are partially related to decreased coronary circulation. Telmisartan may be beneficial in protecting against disturbances in cardiac function associated with metabolic syndrome.

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RETRACTED: Angiotensin receptor blockade improves the net balance of cardiac Ca2+ handling-related proteins in sympathetic hyperactivity-induced heart failure

Abstract: Altogether, these data provide new insights on intracellular Ca(2+) regulatory mechanisms underlying improved ventricular function by ARB therapy in HF.

Cited by 22 publications

References 39 publications

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

Losartan treatment attenuates tumor-induced myocardial dysfunction

Abnormal amounts of intracellular calcium regulatory proteins in SHRSP.Z-Lepr^fa/IzmDmcr rats with metabolic syndrome and cardiac dysfunction

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RETRACTED: Angiotensin receptor blockade improves the net balance of cardiac Ca2+ handling-related proteins in sympathetic hyperactivity-induced heart failure

Abstract: Altogether, these data provide new insights on intracellular Ca(2+) regulatory mechanisms underlying improved ventricular function by ARB therapy in HF.

Cited by 22 publications

References 39 publications

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor

Losartan treatment attenuates tumor-induced myocardial dysfunction

Abnormal amounts of intracellular calcium regulatory proteins in SHRSP.Z-Leprfa/IzmDmcr rats with metabolic syndrome and cardiac dysfunction

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Product

Resources

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Abnormal amounts of intracellular calcium regulatory proteins in SHRSP.Z-Lepr^fa/IzmDmcr rats with metabolic syndrome and cardiac dysfunction