Unexpected Ca2+-mobilization of oxaliplatin via H1 histamine receptors

Potenzieri, A; Riva, Beatrice; Genazzani, Armando A.

doi:10.1016/j.ceca.2019.102128

Cited by 6 publications

(11 citation statements)

References 18 publications

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“…Olodanrigan (EMA401) is a highly selective, orally active angiotensin II type 2 receptor antagonist. It was developed for the therapy of neuropathic pain and in few past years was tested in clinical trials for effectiveness in CIPN patients [140][141][142]. Olodanrigan (EMA401) analgesic action appears to involve inhibition of DRG neuron hyperexcitability.…”

Section: Treatment Strategiesmentioning

confidence: 99%

Prevention and therapy of chemotherapy-induced peripheral neuropathy: a review of recent findings

Michalová

Szekiova

Blasko

et al. 2023

neo

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Chemotherapy-induced peripheral neuropathy is one of the most frequent dose-limiting side effects, observed in patients receiving antineoplastic agents, persisting for up to two years after completing treatment, greatly affecting both the course of chemotherapy and patients' quality of life. Approximately 20 to 85% of patients treated with neurotoxic chemotherapy will develop peripheral neuropathy and there is considerable variability in its severity among patients. The main symptoms are numbness, paresthesia, and burning pain in a "glove and stocking" distribution. The prevalence of chemotherapy-induced peripheral neuropathy will likely increase as cancer survival rates continue to improve. Currently, there are only a few therapeutic options available for the prevention or successful therapy because the mechanisms of chemotherapy-induced peripheral neuropathy remain unclear. A better understanding of the risk factors and underlying mechanisms of chemotherapy-induced peripheral neuropathy is needed to develop effective preventive and therapeutic strategies.

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Section: Treatment Strategiesmentioning

confidence: 99%

Prevention and therapy of chemotherapy-induced peripheral neuropathy: a review of recent findings

Michalová

Szekiova

Blasko

et al. 2023

neo

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“…Brilliant blue G is a P2X7R antagonist, and it suppresses neuroinflammation in subarachnoid hemorrhage animal models, which may be associated with the inhibition of K+ efflux (Chen et al, 2013 ). Therapies targeting Ca2+ and Cl- have also been studied, including U73122 and IAA-94 (Diaz et al, 2013 ; Potenzieri et al, 2020 ). However, therapies targeting ion fluctuations can produce unavoidable side effects caused by the dysregulation of ion-related reactions.…”

Section: Targeting Nlrp3 Inflammasome-related Pathways For the Treatm...mentioning

confidence: 99%

Focus on the Role of the NLRP3 Inflammasome in Multiple Sclerosis: Pathogenesis, Diagnosis, and Therapeutics

Cui

et al. 2022

Front. Mol. Neurosci.

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Neuroinflammation is initiated with an aberrant innate immune response in the central nervous system (CNS) and is involved in many neurological diseases. Inflammasomes are intracellular multiprotein complexes that can be used as platforms to induce the maturation and secretion of proinflammatory cytokines and pyroptosis, thus playing a pivotal role in neuroinflammation. Among the inflammasomes, the nucleotide-binding oligomerization domain-, leucine-rich repeat- and pyrin domain-containing 3 (NLRP3) inflammasome is well-characterized and contributes to many neurological diseases, such as multiple sclerosis (MS), Alzheimer's disease (AD), and ischemic stroke. MS is a chronic autoimmune disease of the CNS, and its hallmarks include chronic inflammation, demyelination, and neurodegeneration. Studies have demonstrated a relationship between MS and the NLRP3 inflammasome. To date, the pathogenesis of MS is not fully understood, and clinical studies on novel therapies are still underway. Here, we review the activation mechanism of the NLRP3 inflammasome, its role in MS, and therapies targeting related molecules, which may be beneficial in MS.

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“…Altered levels of several neurotransmitters are associated with OIPN [ 91 – 93 ]. In OHP-treated rats, the blockade of proinflammatory cytokine receptors results in γ-aminobutyric acid (GABA) function recovery and the cold and mechanical hypersensitivity relief [ 126 ].…”

Section: The Molecular Basismentioning

confidence: 99%

“…Oral EMA401was tested for effectiveness in CIPN patients in clinical trials. Although EMA401 showed anti-neuropathic properties in painful diabetic neuropathy and postherpetic neuralgia patient populations, these trials were terminated or withdrawn due to the observed side effects of EMA401 [ 93 , 94 , 126 , 127 ]. An open-label biomarker study of EMA401 was conducted in a phase II clinical trial of OIPN patients to prove the conceptual use of EMA401 in OIPN.…”

Section: Chemotherapy-induced Peripheral Neuropathy Prevention and Treatment: Therapy Candidates For Oipnmentioning

confidence: 99%

Targeting strategies for oxaliplatin-induced peripheral neuropathy: clinical syndrome, molecular basis, and drug development

Yang

Zhao

Gao

et al. 2021

J Exp Clin Cancer Res

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Oxaliplatin (OHP)-induced peripheral neurotoxicity (OIPN) is a severe clinical problem and potentially permanent side effect of cancer treatment. For the management of OIPN, accurate diagnosis and understanding of significant risk factors including genetic vulnerability are essential to improve knowledge regarding the prevalence and incidence of OIPN as well as enhance strategies for the prevention and treatment of OIPN. The molecular mechanisms underlying OIPN are complex, with multi-targets and various cells causing neuropathy. Furthermore, mechanisms of OIPN can reinforce each other, and combination therapies may be required for effective management. However, despite intense investigation in preclinical and clinical studies, no preventive therapies have shown significant clinical efficacy, and the established treatment for painful OIPN is limited. Duloxetine is the only agent currently recommended by the American Society of Clinical Oncology. The present article summarizes the most recent advances in the field of studies on OIPN, the overview of the clinical syndrome, molecular basis, therapy development, and outlook of future drug candidates. Importantly, closer links between clinical pain management teams and oncology will advance the effectiveness of OIPN treatment, and the continued close collaboration between preclinical and clinical research will facilitate the development of novel prevention and treatments for OIPN.

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Unexpected Ca2+-mobilization of oxaliplatin via H1 histamine receptors

Cited by 6 publications

References 18 publications

Prevention and therapy of chemotherapy-induced peripheral neuropathy: a review of recent findings

Prevention and therapy of chemotherapy-induced peripheral neuropathy: a review of recent findings

Focus on the Role of the NLRP3 Inflammasome in Multiple Sclerosis: Pathogenesis, Diagnosis, and Therapeutics

Targeting strategies for oxaliplatin-induced peripheral neuropathy: clinical syndrome, molecular basis, and drug development

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