Targeting GPCRs, RTKs, and Ion Channels for Pathological Pain and Neuroinflammation Relief

Pathological pain and neuroinflammation are processes that significantly contribute to the development and persistence of several debilitating clinical conditions, such as peripheral neuropathy, fibromyalgia, multiple sclerosis, migraines, neurodegenerative diseases, and others. These conditions involve complex signaling pathways, including the ones activated by G-protein-coupled receptors (GPCRs), receptor tyrosine kinases (RTKs), and ion channels. GPCRs, such as kinin, neuropeptide, and purinergic receptors, for instance, regulate neuronal excitability, glial activation, and the release of inflammatory mediators. RTKs activated by growth factors can promote cell survival and inflammation, supporting the maintenance of neuroinflammation. Ion channels, such as those from the TRP, ASIC and PIEZO families or voltage-gated channels, control the influx of ions that sensitize neurons and glial cells, amplifying pain and inflammation. Understanding the role of these receptors in painful and neuroinflammatory conditions may contribute to the development of effective therapeutic strategies that could improve the life quality of patients.

This Research Topic aims to compile current advances in targeting GPCRs, RTKs, and ion channels as therapeutic strategies for pathological pain and neuroinflammation relief, highlighting their roles in pain and neuroinflammatory signaling pathways, mechanisms of action, and potential for the development of novel analgesic and anti-inflammatory treatments.

This Research Topical invites submissions, including reviews and original preclinical or clinical research, related to the themes:

- signal transduction pathways mediated by GPCRs, RTKs, and ion channels in pain and neuroinflammation processing;

- novel molecules acting in GPCRs, RTKs, or ion channels with analgesic and neuroprotective potential;

- the role of GPCRs, RTKs, and ion channels in mechanisms underlying inflammatory, neuropathic, and nociplastic pain;

- GPCRs, RTKs, and ion channels involved in mechanisms underlying neuroinflammation and neuroimmune responses.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• ... View all formats

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Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Systematic Review
• Technology and Code

Keywords: neuroimmune response, neuroinflammatory pathways, microglial activation, neuroprotective strategies, nociception cell signaling, signal transduction pathways

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.