Inflammasomes are innate immune sensors and receptors that play key pathological roles in the development and progression of numerous diseases. Recent studies have shown that NLRP3 inflammasomes are critical in the pathology of diseases with a high impact on public health, such as musculoskeletal disorders. Musculoskeletal disorders, mainly caused or aggravated by work and the surrounding environment, are locomotor system disorders such as muscles, joints, bones, as well as diseases associated with neurological and circulatory system injuries. Activation of NLRP3 inflammasomes can induce inflammation and pyroptosis, leading to further bodily harm. Therefore, investigating the mechanism and function of NLRP3 inflammasomes, holds great significance and importance for the prevention and treatment of musculoskeletal disorders. This review provides a summary of the activation pathway and mechanism of NLRP3 inflammasomes, and analyzes the role in musculoskeletal disorders such as sarcopenia, osteoporosis and arthritis, with the aim to facilitate the treatment of musculoskeletal disorders.
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http://dx.doi.org/10.13345/j.cjb.230378 | DOI Listing |
Background: Our laboratory has demonstrated that the NLRP3 inflammasome has a critical role in the microglial innate immune response to Alzheimer's disease (AD)-related peptides, triggering the release of cleaved-caspase-1 and IL-1β. NLRP3 activation was found in post-mortem tissue from individuals with AD (Heneka et al., 2013) and in transgenic models of AD (APP/PS1 mice).
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Clinical Laboratory, Norinco General Hospital, Xi'an, Shaanxi, China.
Background: Recent studies show that N6-methyladenosine (m6A) plays an important role in the pathogenesis of the Alzheimer's disease (AD), while the mechanisms involved were studied insufficiently.
Aims: The present study aimed to explore the effect of human insulin-like growth factor 2 (IGF2) mRNA binding proteins 2 (IGF2BP2), one of the m6A-binding proteins on the progression of AD.
Materials & Methods: The mRNA and protein expression level were determined using RT-qPCR and western blot, respectively.
Background: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
View Article and Find Full Text PDFImmunol Invest
January 2025
Traditional Chinese Medicine, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, Heilongjiang, China.
Objective: This study investigated the mechanism of baicalin (BIA) attenuating the inflammatory response and lung injury in mycoplasma pneumoniae pneumonia (MPP) mice.
Methods: MPP mouse models were established and then treated with BIA, azithromycin, or NLRP3 inflammasome activator. Lung wet-to-dry weight (W/D) ratio were weighed.
J Neuroinflammation
January 2025
Department of Neurology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Yishan Road 600, Shanghai, 200233, China.
Background: Alzheimer's disease (AD) is a prevalent neurodegenerative disorder worldwide, and microglia are thought to play a central role in neuroinflammatory events occurring in AD. Chemerin, an adipokine, has been implicated in inflammatory diseases and central nervous system disorders, yet its precise function on microglial response in AD remains unknown.
Methods: The APP/PS1 mice were treated with different dosages of chemerin-9 (30 and 60 µg/kg), a bioactive nonapeptide derived from chemerin, every other day for 8 weeks consecutively.
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