Targeting dorsal root ganglia for chemotherapy-induced peripheral neuropathy: from bench to bedside.

Ther Adv Neurol Disord

Department of Pain Management and Inflammation and Immunity, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.

Published: September 2024

AI Article Synopsis

  • Chemotherapy-induced peripheral neuropathy (CIPN) is a painful condition that increasingly affects cancer survivors but lacks effective treatments and understanding of its biological mechanisms.
  • Research has highlighted the dorsal root ganglia (DRG) as a key player in CIPN, showing how chemotherapy drugs negatively impact sensory neurons in this area, leading to nerve-related symptoms.
  • Although preclinical studies suggest potential pathways for treatment, there is a scarcity of clinical research on direct interventions related to the DRG, indicating a need for further studies to explore effective therapeutic options for CIPN management.

Article Abstract

Chemotherapy-induced peripheral neuropathy (CIPN) is a debilitating condition affecting an increasing number of cancer survivors worldwide. However, insights into its pathophysiology and availability of effective therapies remain lacking. Dorsal root ganglia (DRG) have been studied as a key component of chemotherapeutic drug toxicity and a potential therapeutic target for CIPN treatment. This comprehensive review aims to synthesize, summarize, and correlate the results of both preclinical and clinical studies relevant to the pathophysiology and management of CIPN in relation to the DRG. Design: Review. A thorough literature search was conducted using the terms 'dorsal root ganglion' and 'chemotherapy-induced peripheral neuropathy', along with appropriate variations. Searched databases included PubMed, EMBASE, Medline, Cochrane Library, Wiley Library, and Web of Science. Inclusion criteria targeted all English language, peer-reviewed original research from the inception of these databases to the present year. Review articles, book chapters, and other nonoriginal publications were excluded. Of 134 relevant studies identified, the majority were preclinical studies elucidating how various chemotherapeutic agents, especially taxanes, disrupt neurotransmission, inflammatory processes, and apoptotic pathways within sensory neurons of DRG. Not only do these effects correlate with the presentation of CIPN, but their disruption has also been shown to reduce CIPN symptoms in preclinical models. However, clinical studies addressing DRG interventions are very limited in number and scope at this time. These results reveal various pathways within DRG that may be effective targets for CIPN treatment. While limited, clinical studies do offer promise in the utility of DRG neuromodulation in managing painful CIPN. In the future, clinical trials are needed to assess interventions aimed at these neuronal and nonneuronal pathological targets to better treat this complex condition.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11421407PMC
http://dx.doi.org/10.1177/17562864241252718DOI Listing

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