Cellular Stress in the Pathogenesis of Muscular Disorders—From Cause to Consequence

Mensch, Alexander; Zierz, Stephan

doi:10.3390/ijms21165830

Cited by 12 publications

(10 citation statements)

References 186 publications

(236 reference statements)

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“…In our opinion, the increase in oxidative stress in the EAE model might be more strongly related to the changes, caused by denervation, exerted upon the cytological components of muscle fibers. High levels of reactive oxygen species (ROS) promote skeletal muscle contractile dysfunction, resulting in muscle fatigue [35], which in turn has been linked to muscle fiber degeneration and necrosis [36]. However, we did not observe necrotic muscle fibers in the EAE group in this present study nor in our previous work [13].…”

Section: Discussioncontrasting

confidence: 77%

Transcranial Magnetic Stimulation Improves Muscle Involvement in Experimental Autoimmune Encephalomyelitis

Peña-Toledo

Luque

Ruz-Caracuel

et al. 2021

IJMS

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Skeletal muscle is affected in experimental autoimmune encephalomyelitis (EAE), which is a model of multiple sclerosis that produces changes including muscle atrophy; histological features of neurogenic involvement, and increased oxidative stress. In this study, we aimed to evaluate the therapeutic effects of transcranial magnetic stimulation (TMS) on the involvement of rat skeletal muscle and to compare them with those produced by natalizumab (NTZ). EAE was induced by injecting myelin oligodendrocyte glycoprotein (MOG) into Dark Agouti rats. Both treatments, NTZ and TMS, were implemented from day 15 to day 35. Clinical severity was studied, and after sacrifice, the soleus and extensor digitorum longus muscles were extracted for subsequent histological and biochemical analysis. The treatment with TMS and NTZ had a beneficial effect on muscle involvement in the EAE model. There was a clinical improvement in functional motor deficits, atrophy was attenuated, neurogenic muscle lesions were reduced, and the level of oxidative stress biomarkers was lower in both treatment groups. Compared to NTZ, the best response was obtained with TMS for all the parameters analyzed. The myoprotective effect of TMS was higher than that of NTZ. Thus, the use of TMS may be an effective strategy to reduce muscle involvement in multiple sclerosis.

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Section: Discussioncontrasting

confidence: 77%

Transcranial Magnetic Stimulation Improves Muscle Involvement in Experimental Autoimmune Encephalomyelitis

Peña-Toledo

Luque

Ruz-Caracuel

et al. 2021

IJMS

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“…Muscle-specific ATF4-KO mice are partially and transiently resistant to immobilization-induced muscle atrophy, but, strikingly, they did not exhibit muscle sparing following denervation [ 57 ]. This latter feature appears surprising, since ER-stress response activation is a relevant component of muscle atrophy development after denervation and in cancer cachexia [ 21 , 59 ], in addition to other muscle disorders [ 60 ]. Strikingly, the inhibition of ER stress with the chemical chaperone 4-PBA not only led to accelerated muscle loss in lung cancer-bearing mice, but also to significant muscle atrophy in naïve mice [ 21 ].…”

Section: Master Regulators Of Muscle Atrophymentioning

confidence: 99%

Master Regulators of Muscle Atrophy: Role of Costamere Components

Gorza

Sorge

Seclì

et al. 2021

Cells

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The loss of muscle mass and force characterizes muscle atrophy in several different conditions, which share the expression of atrogenes and the activation of their transcriptional regulators. However, attempts to antagonize muscle atrophy development in different experimental contexts by targeting contributors to the atrogene pathway showed partial effects in most cases. Other master regulators might independently contribute to muscle atrophy, as suggested by our recent evidence about the co-requirement of the muscle-specific chaperone protein melusin to inhibit unloading muscle atrophy development. Furthermore, melusin and other muscle mass regulators, such as nNOS, belong to costameres, the macromolecular complexes that connect sarcolemma to myofibrils and to the extracellular matrix, in correspondence with specific sarcomeric sites. Costameres sense a mechanical load and transduce it both as lateral force and biochemical signals. Recent evidence further broadens this classic view, by revealing the crucial participation of costameres in a sarcolemmal “signaling hub” integrating mechanical and humoral stimuli, where mechanical signals are coupled with insulin and/or insulin-like growth factor stimulation to regulate muscle mass. Therefore, this review aims to enucleate available evidence concerning the early involvement of costamere components and additional putative master regulators in the development of major types of muscle atrophy.

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“…Owing to their contractile activity, high oxygen consumption, and energy demand, skeletal muscles continuously produce moderate levels of ROS, which have essential functions in cellular signaling, by regulating the expression/activity of numerous genes and enzymes. However, the type of effect exerted by ROS is highly dependent on cellular antioxidant systems [ 6 , 51 , 52 , 53 ].…”

Section: Role Of Mitochondria In Neuromuscular Diseasesmentioning

confidence: 99%

An Overview of Mitochondrial Protein Defects in Neuromuscular Diseases

et al. 2021

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Neuromuscular diseases (NMDs) are dysfunctions that involve skeletal muscle and cause incorrect communication between the nerves and muscles. The specific causes of NMDs are not well known, but most of them are caused by genetic mutations. NMDs are generally progressive and entail muscle weakness and fatigue. Muscular impairments can differ in onset, severity, prognosis, and phenotype. A multitude of possible injury sites can make diagnosis of NMDs difficult. Mitochondria are crucial for cellular homeostasis and are involved in various metabolic pathways; for this reason, their dysfunction can lead to the development of different pathologies, including NMDs. Most NMDs due to mitochondrial dysfunction have been associated with mutations of genes involved in mitochondrial biogenesis and metabolism. This review is focused on some mitochondrial routes such as the TCA cycle, OXPHOS, and β-oxidation, recently found to be altered in NMDs. Particular attention is given to the alterations found in some genes encoding mitochondrial carriers, proteins of the inner mitochondrial membrane able to exchange metabolites between mitochondria and the cytosol. Briefly, we discuss possible strategies used to diagnose NMDs and therapies able to promote patient outcome.

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Cellular Stress in the Pathogenesis of Muscular Disorders—From Cause to Consequence

Cited by 12 publications

References 186 publications

Transcranial Magnetic Stimulation Improves Muscle Involvement in Experimental Autoimmune Encephalomyelitis

Transcranial Magnetic Stimulation Improves Muscle Involvement in Experimental Autoimmune Encephalomyelitis

Master Regulators of Muscle Atrophy: Role of Costamere Components

An Overview of Mitochondrial Protein Defects in Neuromuscular Diseases

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