Research progress in immune microenvironment regulation of muscle atrophy induced by peripheral nerve injury

Xiang, Yaoxian; Dai, Junxi; Xu, Lei; Li, Xiaokang; Jiang, Junjian; Xu, Jian‐Guang

doi:10.1016/j.lfs.2021.120117

Cited by 16 publications

(6 citation statements)

References 139 publications

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“…Disability resulting from peripheral nerve injury, such as skeletal muscle atrophy, has attracted increasing interest, particularly among those who are prone to peripheral nerve injury 22 . The molecular mechanisms responsible for the changes that occur after peripheral nerve injury remain largely unknown.…”

Section: Discussionmentioning

confidence: 99%

Ablation of NLRP3 inflammasome attenuates muscle atrophy via inhibiting pyroptosis, proteolysis and apoptosis following denervation

You¹,

Huang²,

Xiang³

et al. 2023

Theranostics

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Rationale:The inflammasome has been widely reported to be involved in various myopathies, but little is known about its role in denervated muscle. Here, we explored the role of NLRP3 inflammasome activation in experimental models of denervation in vitro and in vivo. Methods: Employing muscular NLRP3 specific knock-out (NLRP3 cKO) mice, we evaluated the effects of the NLRP3 inflammasome on muscle atrophy in vivo in muscle-specific NLRP3 conditional knockout (cKO) mice subjected to sciatic nerve transection and in vitro in cells incubated with NLRP3 inflammasome activator (NIA). To evaluate the underlying mechanisms, samples were collected at different time points for RNA-sequencing (RNA-seq), and the interacting molecules were comprehensively analysed. Results: In the experimental model, NLRP3 inflammasome activation after denervation led to pyroptosis and upregulation of MuRF1 and Atrogin-1 expression, facilitating ubiquitin-proteasome system (UPS) activation, which was responsible for muscle proteolysis. Conversely, genetic knockout of NLRP3 in muscle inhibited pyroptosis-associated protein expression and significantly ameliorated muscle atrophy. Furthermore, cotreatment with shRNA-NLRP3 markedly attenuated NIA-induced C2C12 myotube pyroptosis and atrophy. Intriguingly, inhibition of NLRP3 inflammasome activation significantly suppressed apoptosis. Conclusions: These in vivo and in vitro findings demonstrate that during denervation, the NLRP3 inflammasome is activated and stimulates muscle atrophy via pyroptosis, proteolysis and apoptosis, suggesting that it may contribute to the pathogenesis of neuromuscular diseases.

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Section: Discussionmentioning

confidence: 99%

Ablation of NLRP3 inflammasome attenuates muscle atrophy via inhibiting pyroptosis, proteolysis and apoptosis following denervation

You¹,

Huang²,

Xiang³

et al. 2023

Theranostics

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“…Experiments with T cell-deficient mice and activated spleen T cell mice have shown that the adaptive immune response of T cells to release cytokines to damaged muscles promotes the continuous proliferation of skeletal muscle stem cells, and aging may alter the function of T cell-induced muscle precursor cells (MPC), leading to the occurrence of sarcopenia [ 49 ]. Immune aging causes a decrease in the number of muscle stem cells (satellite cells) and transfers muscle stem cells to the fibrogenic phenotype [ 50 ], which disrupts muscle regeneration and leads to muscle atrophy.…”

Section: T Cells and Skeletal Musclementioning

confidence: 99%

The effect of T cell aging on the change of human tissue structure

Xu,

Chen,

Cheng

2024

Immun Ageing

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The trend of aging of the global population is becoming more and more significant, and the incidence of age-related diseases continues to rise.This phenomenon makes the problem of aging gradually attracted wide attention of the society, and gradually developed into an independent research field.As a vital defense mechanism of the human body, the immune system changes significantly during the aging process.Age-induced changes in the body’s immune system are considered harmful and are commonly referred to as immune aging, which may represent the beginning of systemic aging.Immune cells, especially T cells, are the biggest influencers and participants in age-related deterioration of immune function, making older people more susceptible to different age-related diseases.More and more evidence shows that T cells play an important role in the change of human tissue structure after aging, which fundamentally affects the health and survival of the elderly.In this review, we discuss the general characteristics of age-related T cell immune alterations and the possible effects of aging T cells in various tissue structures in the human body.

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“…77 Moreover, infiltrated neutrophils can further promote macrophage inflammatory secretion and result in macrophage phenotype conversion, possibly activate satellite cells, and accelerate muscle repair (Figure 2). 78 The study showed that low-density lipoproteins (LDLs) together with CD68 could reinforce the inflammatory secretion and phagocytosis by macrophages 79,80 ; during this stage, particularly, the release of MPO from neutrophils promoted these bindings by oxidative modification for LDLs 81 and these interactions may exert a crucial role in muscle repair. Similarly, MPO was also an important ligand for CD206, 82 which could regulate the macrophage functions by reducing muscular injury and inflammation.…”

Section: Do Neutrophil S Parti Cipate In Muscle Repair?mentioning

confidence: 99%

Molecular feature of neutrophils in immune microenvironment of muscle atrophy

You

Huang

Xiang

et al. 2022

J Cellular Molecular Medi

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Homeostasis in skeletal muscle is sustained by the balance of functional and physical interactions between muscle and myofibre microenvironment. Various factors, such as ageing, disuse and denervation, tip the balance and induce skeletal muscle atrophy. Skeletal muscle atrophy, which involves complex physiological and biochemical changes, is accompanied by adverse outcomes and even increased mortality. Multiple studies have investigated the role of neutrophils in atrophied skeletal muscles; however, neutrophil intrusion in muscle is still a polemical knot. As technical obstacles have been overcome, people have gradually discovered new functions of neutrophils. The classical view of neutrophils is no longer applicable to their biological characteristics. To date, no clear association between the hidden injurious effect of neutrophil intrusion and muscle atrophy has been convincingly proven. Throughout this review, we have discussed the neutrophil activities that mediate muscle atrophy for distinct disease occurrences. Hopefully, this review will help both clinicians and researchers of skeletal muscle atrophy with relevant targets to further explore efficient medical interventions and treatments.

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Research progress in immune microenvironment regulation of muscle atrophy induced by peripheral nerve injury

Cited by 16 publications

References 139 publications

Ablation of NLRP3 inflammasome attenuates muscle atrophy via inhibiting pyroptosis, proteolysis and apoptosis following denervation

Ablation of NLRP3 inflammasome attenuates muscle atrophy via inhibiting pyroptosis, proteolysis and apoptosis following denervation

The effect of T cell aging on the change of human tissue structure

Molecular feature of neutrophils in immune microenvironment of muscle atrophy

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