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Signal transduction and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Brendan Egan, Adam P. Sharples
In a similar manner to proteolysis, autophagy is likely to be involved in skeletal muscle remodelling in response to exercise. Autophagy occurs through various mechanisms that differ in the way they capture proteins or organelles and deliver them to the lysosome for degradation. Macro-autophagy involves entire regions of the cytosol or specific organelles and protein complexes being engulfed by a vacuole known as an autophagosome, which then fuses with the lysosome. Micro-autophagy involves the direct uptake of cytosolic components into lysosomes. In addition, more selective types of autophagy, known as chaperone-mediated autophagy and chaperone-assisted selective autophagy, are able to degrade specific proteins. Like the concept of protein degradation by the UPS, on first impression, autophagy may seem highly destructive, but autophagic processes are initiated by a single session of exercise (77), and in fact may be required for adaptation to exercise training (78). Conceptually, this can be thought of acute exercise activating signal transduction pathways that increase the turnover of skeletal muscle proteins (i.e. activation of both degradation and synthesis), and this increase in turnover is essential for the remodelling of cellular components such as contractile proteins and the extracellular matrix that occurs with exercise training.
Approach to Vacuolar Myopathy
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
It has been scientifically proven that autophagic dysfunction during the cellular catabolic process is considered the main predisposing factor for vacuolar myopathy. This impairment prevents the elimination of misfolded protein aggregates and increases the ability of cellular oxidative stress. As a result, lysosomal breakdown occurs. Several mechanisms in the literature have explained the pathogenesis of these vacuoles (Figure 15.1). A selective impairment of cargo sequestration is often encountered in vacuolar myopathies. This may cause a defected chaperone-assisted selective autophagy (CASA) that forms protein-containing vacuoles such as myofibrillar myopathies (MFMs).
Autophagy-deficiency in bone marrow mononuclear cells from patients with myasthenia gravis: a possible mechanism of pathogenesis
Published in International Journal of Neuroscience, 2021
Jingqun Tang, Ziming Ye, Yi Liu, Mengxiao Zhou, Liqiang Huang, Qin Mo, Xiaotao Su, Chao Qin
To date, extremely little is known about the effect of autophagy on MG patients. In an experimental autoimmune MG (EAMG) animal model, the activation of CAR3 (the mouse homologue of carbonic anhydrase 3) decreased the degradation of postsynaptic CHRN (cholinergic receptor nicotinic) and further delayed the progression and development of MG by suppressing chaperone-assisted selective autophagy [28]. However, deficient autophagy in BM stem cell of MG patients, which give rise to lymphocytes [23], may even contribute to the pathogenesis of MG. In this study, we aimed to detect the activity of autophagy in bone marrow mononuclear cells (BM-MNCs) from patients with MG before immunomodulation therapy to reveal the possible pathogenesis of MG in bone marrow.