China 
Africa 
Explore chapters and articles related to this topic
Muscle Physiology and Electromyography
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
The interdigitating arrangement of the actin and myosin filaments has a consistent cross-sectional arrangement. Both myofilament types are arranged in a hexagonal pattern, and where there is overlap between the two, the myosin filaments are found in the center of a hexagon of actin filaments (Fig. 7).
The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
In summary, it is clear that studies of the mode of action of angiotensin II on vascular smooth muscle are still at an early stage, and only tentative proposals are possible. Angiotensin II probably contracts vascular smooth muscle by the following sequence of events. The peptide initially combines with specific receptors on the cell membrane surface. This leads to a rise in cytoplasmic calcium concentration, possibly because of increasing plasma membrane permeability or by displacement of the cation from the membrane bound intracellular sites, or both. The rise in cytoplasmic calcium then triggers myofilament contraction in the manner postulated generally for smooth-muscle cells. In addition, combination of angiotensin II with its receptor may lead to a fall in cell cyclic AMP, which could also mediate the rise in Ca2+. The evidence for many of these steps is at present only preliminary.
Past History-Dependence of Myosin Head Performance
Published in Haruo Sugi, Mysteries in Muscle Contraction, 2017
It seems possible that actin filaments are positioned within the myosin filament lattice by electrostatic repulsion forces between the two filaments. Since the electrostatic force is inversely proportional to the square of the interfilament distance, the stretch-induced actin filament displacement from the trigonal position in myosin filament lattice (Fig. 117B) may result in an increase in the overall repulsion forces within the whole myofilament lattice. It is well known that the myofilament lattice in the intact muscle or muscle fiber behaves as a constant-volume system. In the constant-volume myofilament lattice, the stretch-induced increase in the overall electrostatic repulsion forces between the filaments may produce an increase in the force required not only to get them closer together but also to maintain their disordered position.
A review on qualifications and cost effectiveness of induced pluripotent stem cells (IPSCs)-induced cardiomyocytes in drug screening tests
Published in Archives of Physiology and Biochemistry, 2023
Golrokh Malihi, Vahid Nikoui, Elliot L. Elson
Adult cardiomyocytes as a contractile machine are highly organised, and their myofilament proteins need dynamic protein synthesis and turnover. Therefore, to construct myofilament proteins, strict stoichiometry is required. Recently, through advanced techniques of stoichiometric gene replacement with exogenous human cTnl, acquisition of a mature signature in iPSC-CMs could thus be possible. In addition, there are two myosin light chain 2 (MLC2) isoforms including MLC2a and MLC2v, the former presents immature iPSCs and the latter is indicative of mature and adult ventricular cardiomyocytes (O'Brien et al.1993, Kubalak et al.1994). Earlier studies have shown that prevalent double -positive cardiomyocytes for MLC2v/MLC2a with disorganised sarcomeres and not fully developed HERG channel represents immature-like foetal myocytes (Stett et al. 2003). Therefore, hiPSC-CMs expressing MLC2v appear to be ventricular-like cells, while those expressing MLC2a may represent a range of immature cardiac myocytes, including atrial-like cells. The goal is to produce ventricular hiPSC-CMs that fully express cTnI and MLC2v, while they lack ssTnI expression, as in adult myocardium.
Hypertrophic cardiomyopathy: an up-to-date snapshot of the clinical drug development pipeline
Published in Expert Opinion on Investigational Drugs, 2022
Juan Tamargo, María Tamargo, Ricardo Caballero
Pathogenic loss-of-function MYBPC3 mutations represent ~20% of identified HCM mutations and most pathogenic variants encode truncating mutations leading to haploinsufficiency of the MYBPC3 protein [174]. Decreased sarcomeric levels of MYBPC3 result in decreased myosin inhibition with more myosin heads engaged in the actin filament, increased myofilament Ca2+ sensitivity, and hypercontractility. A direct treatment of MYBPC3 haploinsufficiency is the restoration of the insufficient gene product. TN-201 is an adeno-associated virus (AAV) vector which encodes the human gene to selectively restore MYBPC3 in the cardiomyocytes. In a symptomatic murine model, TN-201 dose-dependently reversed cardiac dysfunction and hypertrophy and restored wild-type MYBPC3 protein levels. The cardiac benefit persisted one-year post-injection even in late-stage homozygous disease, and in adult and infant mice injected with >10X no alterations in cardiac function were observed [175]. LX2022 is another investigational agent that delivers one exact copy of the TNNI3 gene via an AAV vector, being indicated for patients with HCM caused by mutations in this gene. Nevertheless, it is too early to advance an opinion of both strategies.
Effect of nebivolol on altered skeletal and cardiac muscles induced by dyslipidemia in rats: impact on oxidative and inflammatory machineries
Published in Archives of Physiology and Biochemistry, 2022
Ghada Farouk Soliman, Omnia Mohamed Abdel-Maksoud, Mohamed Mansour Khalifa, Laila Ahmed Rashed, Walaa Ibrahim, Heba Morsi, Hanan Abdallah, Nermeen Bastawy
Reactive oxygen species (ROS) are important for the regulation of several body functions (Di Meo et al.2016). They are generated in skeletal muscles both during rest and contraction (Powers et al.2011). Mitochondria are major sources of ROS within the striated muscle cell (Görlach et al.2015). The skeletal muscles contain abundant antioxidant Defence system to protect against changes in the redox state. Data exist regarding the deleterious effects of oxidative stress within striated muscle tissues at several levels including cell membrane, sarcoplasmic reticulum, up to myofibrils (Powers et al.2011). Thin filament protein oxidation negatively affects contractile function in striated muscles by reducing calcium sensitivity of the myofilament (Lamb and Westerblad 2011, Steinberg 2013). Changes may occur in titin as a result of oxidative stress in striated muscles (Beckendorf and Linke 2015). Superoxide generated within striated muscle fibres causes oxidation of the ryanodine receptor and, thus, interferes with calcium release (Cherednichenko et al.2004, Xia et al.2003). Glutathione (GSH) is a hydrogen donor formed mainly in the liver, and its reduced form plays important roles in reducing H2O2 and some other cellular antioxidants (Powers et al.2011, Di Meo et al.2016). In addition to diminished expression of cardiac antioxidant enzymes with resultant oxidative stress by the effect of hypercholesterolaemia (Csonka et al.2016).