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Hypertrophic Cardiomyopathy
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Ahmad Masri, Stephen B. Heitner
Sarcomeric mutations in HCM lead to inefficient ATP utilization, resulting in a depleted energy state and a compromise in important homeostatic functions.91 HCM mutation carriers have impaired high-energy phosphate metabolism as evident by reduced phosphocreatine-to-ATP ratio.92 As a compensatory mechanism, there is increased carbohydrate utilization relative to fatty acids (glucose being a more efficient energy source for ATP production)—akin to cardiomyocyte adaptation during ischemia.
Metabolic Cardiology
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
In humans, this metabolic deficit is shown to be greater in compensated left ventricular hypertrophy (with or without concomitant CHF) than in dilated cardiomyopathy.43,44 Hypertensive heart disease alone was not shown to contribute to alterations in high-energy phosphate metabolism, but it can contribute to left ventricular hypertrophy and DD that can later alter cardiac energetics.45,46 Further, for a similar clinical degree of HF, volume overload hypertrophy does not, but pressure overload does, induce significant high-energy phosphate impairment.47,48 This explains why hypertensive patients or patients with aortic valvular disease are so much more vulnerable in the setting of even mild CHF.
Metabolism
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The basic chemical currency of energy in all living cells consists of the two high-energy phosphate bonds contained in ATP. To a lesser extent, other purine and pyrimidine nucleotides (guanosine triphosphate, cytosine triphosphate and inosine triphosphate) also serve as energy sources after energy from ATP is transferred to them. The brain and muscle can use the high-energy phosphate bond in creatine phosphate as a backup store for energy.
Effect of adenosine triphosphate on ribociclib-induced skin toxicity in rats
Published in Cutaneous and Ocular Toxicology, 2023
Nergis Akbaş, Emin Murat Akbaş, Zeynep Süleyman, Betül Çiçek, Ahmet Gökhan Ağgül, Behzad Mokhtare, Halis Süleyman
In our study ATP significantly suppressed the ribociblib-induced MDA increase and decreased the tGSH, SOD, and CAT activity in the skin tissue. SOD and CAT activities are decreased in ribociclib-related damaged skin tissue. There are limited studies in the literature on the effect of ATP on skin damage. Previous studies have reported that ATP protects skin tissue from oxidative damage by sunitinib and vandetanib [10,11]. This reduction in high-energy phosphate concentrations has been reported to result in oxidative stress and LPO [24]. Chiang et al. accelerated the healing of skin tissue by increasing the expression of vascular endothelial growth factor in the scar tissue of mice treated with ATP [25]. Although the mechanisms by which intracellular ATP heals skin damage are not fully understood, it is clear that the presence of ATP plays an important role in the healing process [10,11,25]. The information we obtained from the literature shows that CDK4/6 inhibitors act as an antagonist of ATP and lead to increased oxidative mitochondrial metabolism [26].
Effect of exercise training on cardiac metabolism in rats with heart failure
Published in Scandinavian Cardiovascular Journal, 2020
Tomas Stølen, Mingshu Shi, Martin Wohlwend, Morten A. Høydal, Tone F. Bathen, Øyvind Ellingsen, Morteza Esmaeili
Several lines of evidence suggest that exercise training benefits HF patients both physiologically and psychologically [5,6]. Exercise training can improve myocardium oxidative metabolism, ventricular function, and coronary circulation [7–9]. Remaining challenges include understanding the underlying biology of exercise-related improvements in cardiac performance, including identification of the optimal intensity, frequency, and duration of exercise training for HF patients, and accurate quantification of the associated physiological alterations. Cellular maintenance of high-energy phosphate metabolism seems to be necessary to maintain myocardial function. Many studies suggest that the MI pathogenesis is associated with impaired bioenergetic metabolism and mitochondrial dysfunction [10–13]. Although the molecular mechanisms are not fully understood, it seems that high-energy phosphates are downregulated as a result of abnormal mitochondrial function. The decrease in myocardial phosphocreatine (PCr)/adenosine triphosphate (ATP) ratio in HF patients correlates with the New York Heart Association functional classes, and is a predictor of cardiovascular mortality [14,15]. This finding has raised the possibility that measurements of phosphorous metabolites could be utilized in the evaluation of HF pathogenesis and response to treatment.
Effects of Creatine Supplementation on Muscle Fatigue in Rats Receiving Doxorubicin Treatment
Published in Nutrition and Cancer, 2020
Zoltan A. Torok, Raquel B. Busekrus, David S. Hydock
It has been suggested that creatine supplementation works through a number of distinct mechanisms including increasing skeletal muscle phosphocreatine (PCr) concentrations thereby aiding in the rephosphorylation of adenosine diphosphate (ADP) into adenosine triphosphate (ATP) by the creatine kinase enzymatically driven reaction (8,9). Creatine supplementation can enhance the capacity for high- energy phosphate diffusion between the mitochondria and mysosin heads, which better enables them to engage the contractile protein in cross-bridge cycling and tension maintenance (10). In the 1990’s, Cr supplementation became a popular ergogenic aid to increase exercise performance (11). Since then, Cr has also been used as a therapeutic agent in the treatment of human disease conditions (12). In the past decade, the use of Cr for therapeutic purposes has received increasing attention (13). Creatine supplementation has been beneficial in a large number of muscular, neurological, and cardiovascular diseases (12,14–25); however less documented are the effects of Cr on Dox-induced skeletal muscle dysfunction.