3 edition of Cardiac mitochondrial biogenesis during acute cardiac hypertrophy in the Sprague-Dawley rat found in the catalog.
Cardiac mitochondrial biogenesis during acute cardiac hypertrophy in the Sprague-Dawley rat
Richard E. Albin
Written in English
|Statement||by Richard E. Albin.|
|LC Classifications||Microfilm 40160 (Q)|
|The Physical Object|
|Pagination||vii, 126 leaves|
|Number of Pages||126|
|LC Control Number||88893506|
Although postnatal Hx is known to acutely worsen mitochondrial dysfunction and oxidative stress in the lung, relative hyperoxia, as is encountered at birth into a normoxic environment, is critical to initiate neonatal cardiac mitochondrial biogenesis and oxidative metabolism within the LV (35–38). However, the acute and chronic effects of. Nitric oxide synthase-2 induction optimizes cardiac mitochondrial biogenesis after endotoxemia. Free Radic Biol Med –, Crossref PubMed ISI Google Scholar; Rinaldi S, Landucci F, De Gaudio AR. Antioxidant therapy in critically septic patients. Curr Drug Targets –, Crossref PubMed ISI Google Scholar;
Introduction. Congestive heart failure is a complex syndrome, which includes disturbances in ventricular function, neurohumoral and cytokine activation and increased arrhythmias (Hasenfuss and Pieske, ; Jessup and Brozena, ).Accumulating evidence indicates a central role for myocyte mishandling of calcium in the pathogenesis of heart failure (del Monte and Hajjar, ). Heart failure is a major cause of death throughout the world. Hyperthyroidism has been shown to induce cardiac hypertrophy, which is a contributing factor to heart failure. However, the mechanism underling effect of thyroid hormone is not completely clear. The present study investigates the role of peroxisome proliferator‐activated receptor (PPAR) γ coactivator‐1α (PGC‐1α) in cardiac.
Diabetes mellitus is an important risk factor for atrial fibrillation (AF) development. Sodium–glucose co-transporter-2 (SGLT-2) inhibitors are used for the treatment of type 2 diabetes mellitus (T2DM). Their cardioprotective effects have been reported but whether they prevent AF in T2DM patients are less well-explored. We tested the hypothesis that the SGLT-2 inhibitor, empagliflozin, can. Neonatal rat cardiomyocytes (NRCs) were isolated from the ventricles of 1‐ to 2‐day‐old Sprague–Dawley rat pups as previously described. 17 Ventricular tissues of rat pups were digested with collagenase at 37°C overnight, followed by further digestion in trypsin.
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Thus, the increased ROS during hypertrophy [7, 8, 9, 27] and the attenuation of cardiac hypertrophy with antioxidants [5, 26, 27, ] is a strong point for the implication of mitochondrial oxidative stress on cardiac hypertrophy/heart failure since mitochondria are the main intracellular source of ROS in by: Oxidative stress-induced redox imbalance in the cardiomyocytes is one of the primary reasons for the development of myocyte hypertrophy .
Mitochondria are responsible for the generation of~95%. Mitochondrial biogenesis enzymes. The protein expression levels of cytochrome C and succinate dehydrogenase were measured to evaluate the effects of diet and/or exercise on mitochondrial biogenesis within the cardiac muscle.
Eight weeks of ladder-climbing exercise significantly increased the mitochondrial enzyme levels (pCited by: 2. Interestingly, these proteins are known to change in abundance during cardiac hypertrophy in vitro and have also been shown to change in human/animal models of hypertrophy.
Proteomic analysis revealed significant elevation of heat shock protein 70 in patients with chronic heart failure due to arrhythmogenic right ventricular cardiomyopathy (ARVC).Cited by: In the present study we explored whether raw garlic and its compound, diallyl disulfide (DADS) could inhibit hypertrophy through H2S and/or mitochondrial biogenesis.
Cardiac hypertrophy was. during the progression of cardiac hypertrophy, there is a shift from fatty acid oxidation (FAO) toward increased glucose oxidation resembling the fetal metabolic program (2, 35).Initially, this metabolic switch may be adaptive and protective to maintain contractile function; however, this subsequently becomes one of the etiological components in the development of decompensation and heart failure.
J Mol Cell CardiolAlbin R, Dowell T, Zak R, et al: Synthesis and turnover of cytochrome c in cardiac hypertrophy. Circ Res, in press Albin R: Cardiac mitochondrial biogenesis during acute car- diac hypertrophy in Sprague-Dawley rat.
PhD thesis, Uni- versity of Chicago,p Mitochondria are at the centre of cardiac energy metabolism, since they satisfy ∼90% of heart's daily energy requirements through oxidative phosphorylation.
Indeed, in the failing heart, mitochondria were shown to undergo pathological structural and functional remodelling. mRNA and protein expression of genes regulating mitochondrial biogenesis decreased in systolic dysfunction; PCr/ATP ratio decreased: SHRs (Sprague-Dawley rats as controls) Hypertrophy, heart function ex vivo unchanged: FAO lower (note that some strains of SHRs have a mutation in CD36, which could independently modulate FAO) GO higher: At present, the treatment of heart failure has entered the plateau phase, and it is necessary to thoroughly study the pathogenesis of heart failure and find out the corresponding treatment methods.
Myocardial mitochondria is the main site of cardiac energy metabolism, whose dysfunction is an important factor leading to cardiac dysfunction and heart failure. Mitochondria are highly dynamic. In contrast, in cardiac tissue, HDAC inhibitors have been shown to suppress cardiac hypertrophy and I/R injury and protect against cell death [17,43].
Furthermore, inhibitors of Class I HDACs enhance mitochondrial biogenesis and oxidative metabolism in skeletal muscle and adipose tissue. Collectively, these results suggest that responses to. Also, cardiac hypertrophy was induced in Sprague–Dawley rats by Ang II, and the effect of increasing HETE by isoniazid (INH; mg/kg/day) was assessed by heart weight and echocardiography.
Also, alterations in cardiac cytochrome P (CYP) and their associated arachidonic acid (AA) metabolites were determined by real-time PCR, Western.
or direct phosphorylation of PGC-1α . In addition, inhibition of hypertrophy  and cardiac fibrosis  induced by AMPK activation was associated with enhanced PPARα activity.
However, the contribution of the activation of AMPK/PPARα pathway to prevent cardiac and mitochondrial dysfunctions in acute IR remains to be elucidated.
On one hand, diabetes impairs myocardial mitochondrial biogenesis, leading to loss of mitochondrial number and function, which eventually causes cardiac contractile dysfunction 5,6. Mitochondrial biogenesis is enhanced during the cardiomyocyte compensated hypertrophy phase in an effort to match energy demand, but is subsequently decreased during the pathological decompensation phase.
δ-Sarcoglycan null hamsters, a rodent model of dilated cardiomyopathy that exhibits decreased mitochondrial oxidative capacity and is. Akt and Gsk-3β are positive and negative regulators of cardiac hypertrophy, respectively.
10 Akt phosphorylation and activation is directly involved in the modulation of cardiac hypertrophy by. Musa balbisiana Colla (Family: Musaceae), commonly known as banana and native to India and other parts of Asia, is very rich in nutritional value and has strong antioxidant potential.
In the present study, we have developed Musa balbisiana (MB) fruit pulp powder and evaluated its cardioprotective effect in cardiac hypertrophy, which is often associated with inflammation and oxidative stress.
Intrinsic cardiac aging in the murine model closely recapitulates age-related cardiac changes in humans, including left ventricular hypertrophy, fibrosis and diastolic dysfunction.
Cardiac aging in mice is accompanied by accumulation of mitochondrial protein oxidation, increased mitochondrial DNA mutations, increased mitochondrial biogenesis.
Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult.
Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Cardiac Hypertrophy Mitochondrial Biogenesis Heart Mitochondrion Physiol Heart Circ Adenine Nucleotide Translocator These keywords were added by machine and not by the authors.
This process is experimental and the keywords may be updated as the learning algorithm improves. The effect of nanoSiO 2 perfusion on cardiac function was studied in isolated rat hearts.
Exposing the perfused hearts to μg/mL resulted in accumulation on the apex, as evidenced in Fig. 1a. The RPP response was evaluated during 60 min using Krebs-Henseleit buffer with or without nanoSiO2, see Fig. 1b. The perfused group with nanoSiO 2, with respect to the NT group, showed a sigmoidal.Mitochondrial aberrations have been linked to numerous aspects of cardiovascular disease, such as ischemia reperfusion injury, 21 cardiomyopathy, 22 and heart failure.
24 In fact, mitochondrial dysfunction purportedly contributes to the development of cardiac hypertrophy vis-à-vis, for example, altered mitochondrial biogenesis, decreased. Introduction. Type 2 diabetes mellitus (T2DM) and heart failure (HF) commonly coexist.
1 Patients with T2DM have a two‐fold increased risk of developing HF during their lifetime, 2, 3 and are also twice as likely to be hospitalized for HF. Cardiovascular events and HF hospitalizations can be reduced by adequate glycaemic control in patients with T2DM, 7 but once HF develops the.