Molecular Signaling Pathways in Acute and Chronic Inflammation and Pain

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1270

Special Issue Editor


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Guest Editor
Department of Anesthesiology, Chi Mei Medical Center, Tainan; School of Medicine, College of Medicine, National SunYat-sen University, Kaohsiung, Taiwan
Interests: inflammation; pain; immunity

Special Issue Information

Dear Colleagues,

Emerging research indicates that nociceptor neurons may have a significant impact on the immune response and inflammation. This suggests that pain is not only a prominent feature of inflammation but that it also plays a crucial role in regulating the immune system. When exposed to noxious stimuli, nociceptors can release neuropeptides and neurotransmitters that exert potent regulatory effects on the vasculature, as well as on innate and adaptive immunity. Various immune cells, including dendritic cells, neutrophils, macrophages, mast cells, and T cells, possess receptors for these neuronal mediators, enabling direct responses to nociceptors. It is increasingly evident that interactions between nociceptor neurons and the immune system are pivotal in both pain perception and inflammation. The dysregulation of these interactions could potentially underlie the development of inflammatory conditions affecting the skin, joints, respiratory system, and gastrointestinal tract. Furthermore, these neuroimmune interactions have been observed in peripheral tissues of damage as well as in the central nervous system. Understanding the interplay between nociceptors, immune cells, and glial cells can aid in the discovery of novel mechanisms underlying inflammatory disorders, and in the development of innovative therapeutics to treat and prevent inflammatory diseases and chronic pain. While several molecules may contribute to the onset of acute and chronic inflammation and pain, their precise mechanisms have not yet been elucidated. More recently, our understanding of the molecular mechanisms initiating the resolution of inflammation and pain has opened up new avenues for strategies aimed at managing complex acute and chronic inflammatory diseases and pain. However, it is important to note that resolution pathways are diverse and likely vary depending on the specific tissue and stimulus involved.

In the context of this Special Issue, we welcome submissions of original research and reviews pertaining to acute and chronic inflammation as well as pain. We specifically encourage contributions that emphasize the molecular mechanisms underlying the persistence of inflammation and pain, in contrast to their resolution.

Dr. Ping-Heng Tan
Guest Editor

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Keywords

  • inflammation
  • pain
  • immune response
  • nervous system
  • molecular mechanism

Published Papers (1 paper)

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Review

15 pages, 2138 KiB  
Review
Molecular and Cellular Involvement in CIPN
by Housem Kacem, Annamaria Cimini, Michele d’Angelo and Vanessa Castelli
Biomedicines 2024, 12(4), 751; https://doi.org/10.3390/biomedicines12040751 - 28 Mar 2024
Viewed by 1057
Abstract
Many anti-cancer drugs, such as taxanes, platinum compounds, vinca alkaloids, and proteasome inhibitors, can cause chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a frequent and harmful side effect that affects the sensory, motor, and autonomic nerves, leading to pain, numbness, tingling, weakness, and reduced [...] Read more.
Many anti-cancer drugs, such as taxanes, platinum compounds, vinca alkaloids, and proteasome inhibitors, can cause chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a frequent and harmful side effect that affects the sensory, motor, and autonomic nerves, leading to pain, numbness, tingling, weakness, and reduced quality of life. The causes of CIPN are not fully known, but they involve direct nerve damage, oxidative stress, inflammation, DNA damage, microtubule dysfunction, and altered ion channel activity. CIPN is also affected by genetic, epigenetic, and environmental factors that modulate the risk and intensity of nerve damage. Currently, there are no effective treatments or prevention methods for CIPN, and symptom management is mostly symptomatic and palliative. Therefore, there is a high demand for better understanding of the cellular and molecular mechanisms involved in CIPN, as well as the development of new biomarkers and therapeutic targets. This review gives an overview of the current knowledge and challenges in the field of CIPN, focusing on the biological and molecular mechanisms underlying this disorder. Full article
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