Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α

Tyagi, Sidharth; Higerd-Rusli, Grant P.; Ghovanloo, Mohammad-Reza; Dib-Hajj, Fadia; Zhao, Peng; Liu, Shujun; Kim, Dong-Hyun; Shim, Ji Seon; Park, Kang-Sik; Waxman, Stephen G.; Choi, Jin-Sung; Dib-Hajj, Sulayman D.

doi:10.1016/j.celrep.2024.113685

Cited by 7 publications

(2 citation statements)

References 86 publications

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“…Hyperphosphorylation of Nav1.7 contributes to its insertion into the somatic membrane of neurons. 347 The expression of Nav1.8 and Nav1.9 is meanwhile upregulated. 348 MAPK-ERK-CREB signaling has also been found to increase Nav1.6 expression in the oxaliplatin-induced neuropathic pain model.…”

Section: Molecular Mechanisms Of Pain Modulationmentioning

confidence: 99%

Pathology of pain and its implications for therapeutic interventions

Cao,

Xu,

Shi

et al. 2024

Sig Transduct Target Ther

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Pain is estimated to affect more than 20% of the global population, imposing incalculable health and economic burdens. Effective pain management is crucial for individuals suffering from pain. However, the current methods for pain assessment and treatment fall short of clinical needs. Benefiting from advances in neuroscience and biotechnology, the neuronal circuits and molecular mechanisms critically involved in pain modulation have been elucidated. These research achievements have incited progress in identifying new diagnostic and therapeutic targets. In this review, we first introduce fundamental knowledge about pain, setting the stage for the subsequent contents. The review next delves into the molecular mechanisms underlying pain disorders, including gene mutation, epigenetic modification, posttranslational modification, inflammasome, signaling pathways and microbiota. To better present a comprehensive view of pain research, two prominent issues, sexual dimorphism and pain comorbidities, are discussed in detail based on current findings. The status quo of pain evaluation and manipulation is summarized. A series of improved and innovative pain management strategies, such as gene therapy, monoclonal antibody, brain-computer interface and microbial intervention, are making strides towards clinical application. We highlight existing limitations and future directions for enhancing the quality of preclinical and clinical research. Efforts to decipher the complexities of pain pathology will be instrumental in translating scientific discoveries into clinical practice, thereby improving pain management from bench to bedside.

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Section: Molecular Mechanisms Of Pain Modulationmentioning

confidence: 99%

Pathology of pain and its implications for therapeutic interventions

Cao,

Xu,

Shi

et al. 2024

Sig Transduct Target Ther

View full text Add to dashboard Cite

show abstract

“…The PXY motif in the C-terminus of multiple Na V channels also recruits NEDD4-2 ubiquitin ligases and induces their internalization ( 22 ). Activation of p38 MAPK by treatment of DRG neurons with TNF-α causes phosphorylation of a SP dipeptide in the N-terminus of Na V 1.7, which alters insertion of channels in the plasma membrane ( 24 ). Another example of the modulation of channel density is provided by the observation that treatment of DRG neurons with anisomycin causes an increase in Na V 1.8 current density in a p38 MAPK dependent manner, due to the phosphorylation of SP dipeptides in the L1 of the channel ( 25 ).…”

Section: Strategies For Reducing Nav Channel Expressionmentioning

confidence: 99%