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Metabolic Cardiology
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The energy-starved heart is often not considered by physicians who treat cardiac disease on a day-to-day basis. Angiotensin-converting enzyme inhibitors and angiotensin receptor II blockers improve survival in ischemic and non-ischemic HFs and should be considered as a conventional approach in any patient with heart failure. However, therapies that target the cardiomyocyte itself must also be employed as it has been shown that cardiomyocytes in the failing heart, although metabolically compromised, and their function can be potentially improved and restored. Therapies that go beyond symptomatic relief (diuretics), and the neurohormonal axis, must also be considered that target the cellular, mitochondrial and metabolic defects. Metabolic support with D-ribose, CoQ10, L-carnitine and magnesium is critical for the maintenance of contractile reserve and energy charge in minimally oxidative ischemic or hypoxic hearts. Preservation of cellular energy charge provides the chemical driving force required to complete ATPase reactions needed to maintain cell and tissue viability and function. D-ribose, CoQ10, L-carnitine and magnesium exert a physiological benefit that has a positive impact on cardiac function.
Exercise Redox Signalling
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Ruy A. Louzada, Jessica Bouviere, Rodrigo S. Fortunato, Denise P. Carvalho
In the onset of muscle contraction, a high demand for ATP drives the cellular metabolism to provide energy for ATPases, calcium handling events, and promotion of the crossbridge interaction between actin and myosin filaments. Within milliseconds, ATP demand rapidly induces an orchestrated metabolic flow to match the demand for ATP. Initially, mitochondria were believed to be the main source of ROS following exercise based on an obvious correlation between increased oxygen consumption and increased ATP production. It has been shown that at least 11 mitochondrial sites can generate ROS in mammals that depends on the bioenergetic state (Wong et al., 2017). Remarkably, during exercise mitochondria operate in state 3 (also known as the maximal ADP stimulated respiration) and thereby reduce ROS generation, contrary to what is observed in the basal conditions, where mitochondria operate in respiration state 4 (Goncalves et al., 2015). Elegantly, when mitochondria are exposed to a condition that mimics exercise, H2O2 is considerably reduced (Goncalves et al., 2015; Jackson et al., 2016) and also confirmed using an in vivo mice model of exercise (Henríquez-Olguin et al., 2019).
Stress Proteins in Renal Ischemia
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
The HSP 70 delivery of unfolded proteins to the rough endoplasmic reticulum for translocation, the binding of HSP 70 to unfolded protein, and the role of HSP 70 in protection, reactivation, and disaggregation are all dependent on ATP 45,46,52–54 HSP 70 is an ATPase. Eisenberg and Green find tenfold stimulation of HSC 70 ATPase by addition of clathrin baskets while Sadis has shown that apocytochrome stimulates HSC 70 ATPase activity but the folded protein cytochrome c does not.8
Kolaviron modulates dysregulated metabolism in oxidative pancreatic injury and inhibits intestinal glucose absorption with concomitant stimulation of muscle glucose uptake
Published in Archives of Physiology and Biochemistry, 2023
Veronica F. Salau, Ochuko L. Erukainure, Neil A. Koorbanally, Md. Shahidul Islam
Purinergic enzymes catalyse the production of adenosines which are involved in the attenuation of inflammation and tissue injury (Ademiluyi et al.2016). ATPase is a purinergic enzyme that catalyses the phospho-hydrolysis of adenosine triphosphate (ATP) to ADP. Ca2+ -Mg2+ -ATPase has been implicated in intracellular calcium homeostasis, as it regulates the inflow of Ca2+ through the cell membrane into the cell. High calcium overload has been implicated in production of pro-inflammatory mediators which is strongly linked to a decrease in the activity of Ca2+ -Mg2+ -ATPase (Qiu et al.2004). Increased production of free radicals during pancreatic injury leads to a redistribution of membrane phospholipids and thus, a contributory factor to the inhibition of ATPase activity (Bruce and Elliott 2007, Mukherjee et al.2008). In the present study, the decreased ATPase activity in the untreated pancreatic tissue (Figure 8(B)) which corroborates induction of oxidative stress (Figure 6) may insinuate Ca2+ overload and inflammation. Treatment with kolaviron increased the activity of ATPase which may indicate an anti-inflammatory role of kolaviron as supported by the decreased NO levels in treated tissues (Figure 7) and suppression of oxidative stress (Figure 6).
An evaluation of mavacamten for the treatment of symptomatic obstructive hypertrophic cardiomyopathy in adults
Published in Expert Review of Cardiovascular Therapy, 2023
Tiffany Dong, Steven Nissen, Susan Ospina, Milind Y Desai
Mavacamten is a first-in-class drug that inhibits cardiac myosin. Mavacamten binds allosterically to the ß-cardiac myosin ATPase and prevents the formation of the myosin-actin bridges. Under normal conditions, ATPase binds ATP to myosin heads and ATP is hydrolyzed to ADP, which leads to myosin-actin binding. Once these bridges are released as the sarcomeres slide past each other ultimately leading to myocardial contraction. Hypercontractility is central to the pathophysiology of HCM, which has about 20% fewer inactive myosin heads compared to normal controls [11]. Thus, mavacamten directly decreases contractility. This drug also prevents the rate limiting step of phosphate release, decreases the rate at which myosin binds to actin and improves ventricular compliance [12,13]. Overall as outlined, mavacamten has multiple mechanisms that lessens sarcomeric force and myocardial contractility.
Himalayan poisonous plants for traditional healings and protection from viral attack: a comprehensive review
Published in Toxin Reviews, 2022
Shriya Pathania, Diksha Pathania, Priyanka Chauhan, Mamta Sharma
The neuroactive alkaloids can function as an agonist which excites a neuroreceptor or can function as an antagonist which blocks a certain neuroreceptor. Receptors on neuron cells are another major target for most alkaloids. These structurally resemble endogenous neurotransmitters such as glutamate, dopamine, acetylcholine, noradrenaline, and adrenaline (Mutschler et al. 2008). A few alkaloids repress the catalysts that separate synapses, like cholinesterase and monoamine oxidase. Neurotoxins also affect significant ion channel of neuronal cells, which includes Na+, K+ and Ca2+ channels, whichever by activating or inactivating them eternally. This activity stops neuronal signal transduction and blocks the activity of the nervous system and neuromuscular. The sodium, potassium ion ATPase is a significant ion pump in neuronal and other cells to keep an ion gradient important for action potentials and transport mechanisms (Wink 2000).