Publications by authors named "D Miranda-Silva"

Article Synopsis
  • Low levels of triiodothyronine (T3) are prevalent in heart failure (HF) patients, and this study aimed to assess the effects of low and replacement doses of T3 in a rat model of HF with preserved ejection fraction (HFpEF).
  • Four groups were evaluated: lean control rats, obese rats with HFpEF, and two groups of obese rats treated with either low or replacement doses of T3, administered via drinking water over 11 weeks.
  • Results indicated that T3 treatment improved metabolic profiles and cardiac function, with the high T3 dose restoring myocardial T3 levels and yielding benefits in calcium handling and heart function, despite no change in overall exercise capacity (VOmax).
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Heart failure (HF) triggered by cardiovascular and non-cardiovascular diseases is a leading cause of death worldwide and translational research is urgently needed to better understand the mechanisms of the failing heart. For this purpose, rodent models of heart disease combined with cardiac functional assessment have provided valuable insights into the physiological significance of a given genetic or pharmacological modification. In small animals, cardiac function and structure can be evaluated by methods such as echocardiography, telemetry or hemodynamics using conductance catheters.

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To better understand the left ventricular (LV) reverse remodeling (RR), we describe a rodent model wherein, after aortic banding-induced LV remodeling, mice undergo RR upon removal of the aortic constriction. In this paper, we describe a step-by-step procedure to perform a minimally invasive surgical aortic debanding in mice. Echocardiography was subsequently used to assess the degree of cardiac hypertrophy and dysfunction during LV remodeling and RR and to determine the best timing for aortic debanding.

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Heart failure with preserved ejection fraction (HFpEF) is a multifaceted syndrome with a complex aetiology often associated with several comorbidities, such as left ventricle pressure overload, diabetes mellitus, obesity, and kidney disease. Its pathophysiology remains obscure mainly due to the complex phenotype induced by all these associated comorbidities and to the scarcity of animal models that adequately mimic HFpEF. Increased oxidative stress, inflammation, and endothelial dysfunction are currently accepted as key players in HFpEF pathophysiology.

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This study aims to provide new insights into transcriptome and miRome modifications occurring in cardiac reverse remodelling (RR) upon left ventricle pressure-overload relief in mice. Pressure-overload was established in seven-week-old C57BL/6J-mice by ascending aortic constriction. A debanding (DEB) surgery was performed seven weeks later in half of the banding group (BA).

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