Mechanisms of Pain Development and Treatment Strategies

Dear Colleagues,

Pain is a complex and heterogeneous pathological condition arising from diverse molecular and cellular processes in the peripheral and central nervous systems. Recent advances in research have revealed that neuroimmune signaling, intracellular stress responses, mitochondrial dysfunction, ion channel dysregulation, neuron–glial interactions, and maladaptive synaptic plasticity play important roles in the onset and persistence of chronic pain. Furthermore, the impact of changes in functional connectivity in the central nervous system resulting from these pathological conditions is also becoming clearer.

These mechanisms are particularly important in neuropathic pain, fibromyalgia, and long COVID/post-COVID-19 sequelae, post-viral fatigue/pain syndrome, suggesting the sharing of crucial pathophysiological pathways.

This Special Issue focuses on the molecular mechanisms of chronic pain onset and the resulting changes in neural networks, with particular attention paid to fibromyalgia, long COVID, post-viral fatigue/pain syndrome and neuropathic pain. Topics covered include, but are not limited to, neuroinflammation, glial cell activation, intracellular stress signaling, mitochondrial and metabolic dysfunction, small fiber neuropathy, synaptic plasticity, central sensitization, alterations in neural networks, opioid tolerance and novel therapeutic approaches targeting these mechanisms.

This Special Issue welcomes submissions of original research papers, reviews, and hypotheses related to basic molecular and cellular research, animal models, translational research, and clinical research. The aim of this Special Issue is to deepen our understanding of the mechanisms of pain disorders and to promote the development of more effective, mechanism-based therapeutic strategies.

Prof. Dr. Tomohiko Aoe
Guest Editor

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