Chronic pain is an unresolved health issue affecting approximately a quarter of adults worldwide. In contrast to acute pain, which has important warning and protection functions, chronic pain is a maladaptive mechanism that continues long after recovery from an injury or disease. Treatment of chronic pain focuses on removing the underlying cause of pain and management of pain symptoms with analgesics. Side effects of analgesia are common and novel targets and medication are urgently needed. Accumulating evidence suggests that neuroinflammation plays a crucial role in the development of chronic pain. Neuroinflammation is triggered by the activation of non-neuronal cells, such as microglia and astrocytes, leading to the secretion of proinflammatory molecules. In addition to causing central sensitization and chronic pain, proinflammatory molecules also attract peripheral immune cells into the tissue, perpetuating inflammation.
The goal of this Research Topic is to explore underlying mechanisms and signalling pathways in chronic pain and neuroinflammation. Research investigating molecular signalling pathways (genetic and epigenetic) and regulation of cellular components is of particular interest to inform the therapeutic approach for chronic pain.
Original research articles involving in vitro/in vivo/ex-vivo/3D organoid culture data, novel or re-examined multi-omics analyses based on integrated genomics/epigenomics/transcriptomics with experimental validation or correlated with electrophysiological features, and recent advances in clinical trials will be of interest. Articles on alternative machine learning methods to extract clinically relevant information are also welcome. Perspective and Review articles focusing on, but not limited to, the following topics will be considered:
- Molecular and cellular mechanisms in chronic pain
- Investigation of molecular and cellular pathways in neuroinflammation and neuroinflammatory signalling
- Communication between non-neuronal cells in the central nervous system and the peripheral immune system
- Activation states of non-neuronal and immune cells
- The role of pro-inflammatory signalling molecules such as cytokines, chemokines and lipid mediators in perpetuating pain
Chronic pain is an unresolved health issue affecting approximately a quarter of adults worldwide. In contrast to acute pain, which has important warning and protection functions, chronic pain is a maladaptive mechanism that continues long after recovery from an injury or disease. Treatment of chronic pain focuses on removing the underlying cause of pain and management of pain symptoms with analgesics. Side effects of analgesia are common and novel targets and medication are urgently needed. Accumulating evidence suggests that neuroinflammation plays a crucial role in the development of chronic pain. Neuroinflammation is triggered by the activation of non-neuronal cells, such as microglia and astrocytes, leading to the secretion of proinflammatory molecules. In addition to causing central sensitization and chronic pain, proinflammatory molecules also attract peripheral immune cells into the tissue, perpetuating inflammation.
The goal of this Research Topic is to explore underlying mechanisms and signalling pathways in chronic pain and neuroinflammation. Research investigating molecular signalling pathways (genetic and epigenetic) and regulation of cellular components is of particular interest to inform the therapeutic approach for chronic pain.
Original research articles involving in vitro/in vivo/ex-vivo/3D organoid culture data, novel or re-examined multi-omics analyses based on integrated genomics/epigenomics/transcriptomics with experimental validation or correlated with electrophysiological features, and recent advances in clinical trials will be of interest. Articles on alternative machine learning methods to extract clinically relevant information are also welcome. Perspective and Review articles focusing on, but not limited to, the following topics will be considered:
- Molecular and cellular mechanisms in chronic pain
- Investigation of molecular and cellular pathways in neuroinflammation and neuroinflammatory signalling
- Communication between non-neuronal cells in the central nervous system and the peripheral immune system
- Activation states of non-neuronal and immune cells
- The role of pro-inflammatory signalling molecules such as cytokines, chemokines and lipid mediators in perpetuating pain
