Endoplasmic Reticulum Stress in Chemotherapy-Induced Peripheral Neuropathy: Emerging Role of Phytochemicals

Goel, Yugal; Fouda, Raghda; Gupta, Kalpna

doi:10.3390/antiox11020265

Cited by 6 publications

(11 citation statements)

References 164 publications

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“…ER stress has an important role in the induction of pain, particularly in neuropathic pain conditions [11,12,75]. Neuropathic pain, often resulting from nerve damage or a malfunctioning nervous system, is notoriously difficult to treat [12,75,76]. The role of ER stress in pain is not limited to neuropathic pain but extends to various medical conditions, including diabetes-induced neuropathic pain, inflammatory pain, and pain associated with diseases like osteoarthritis and viral infection.…”

Section: Er Stress In Pain Inductionmentioning

confidence: 99%

Unraveling the Connection: Pain and Endoplasmic Reticulum Stress

Kawanaka,

Jin,

Aoe

2024

IJMS

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Pain is a complex and multifaceted experience. Recent research has increasingly focused on the role of endoplasmic reticulum (ER) stress in the induction and modulation of pain. The ER is an essential organelle for cells and plays a key role in protein folding and calcium dynamics. Various pathological conditions, such as ischemia, hypoxia, toxic substances, and increased protein production, may disturb protein folding, causing an increase in misfolding proteins in the ER. Such an overload of the folding process leads to ER stress and causes the unfolded protein response (UPR), which increases folding capacity in the ER. Uncompensated ER stress impairs intracellular signaling and cell function, resulting in various diseases, such as diabetes and degenerative neurological diseases. ER stress may be a critical universal mechanism underlying human diseases. Pain sensations involve the central as well as peripheral nervous systems. Several preclinical studies indicate that ER stress in the nervous system is enhanced in various painful states, especially in neuropathic pain conditions. The purpose of this narrative review is to uncover the intricate relationship between ER stress and pain, exploring molecular pathways, implications for various pain conditions, and potential therapeutic strategies.

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Section: Er Stress In Pain Inductionmentioning

confidence: 99%

Unraveling the Connection: Pain and Endoplasmic Reticulum Stress

Kawanaka,

Jin,

Aoe

2024

IJMS

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“…Neuroprotective drugs including duloxetine, amifostine, B vitamins, antioxidants such as vitamin E, alpha‐lipoic acid, glutathione and glutamine, and minocycline have certain effects on the prevention and treatment of CIPN. However, evidence‐based medicine is insufficient, and it can be used clinically as appropriate 102–104 . The American Society of Clinical Oncology (ASCO) guidelines states that duloxetine as a serotonin–norepinephrine reuptake inhibitor is the only recommended treatment 6 .…”

Section: Treatment Of Cipn After Chemotherapy For Hematological Malig...mentioning

confidence: 99%

“…However, evidence‐based medicine is insufficient, and it can be used clinically as appropriate. 102 , 103 , 104 The American Society of Clinical Oncology (ASCO) guidelines states that duloxetine as a serotonin–norepinephrine reuptake inhibitor is the only recommended treatment. 6 Neurotropine has been reported to reverse paclitaxel‐ and OXP‐induced CIPN in rats.…”

Section: Treatment Of Cipn After Chemotherapy For Hematological Malig...mentioning

confidence: 99%

Animal models of chemotherapy‐induced peripheral neuropathy for hematological malignancies: A review

Mao

Cao

et al. 2022

Ibrain

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Chemotherapy is one of the main treatments for hematologic malignancies.However, chemotherapy-induced peripheral neuropathy (CIPN) is one of the most common long-term toxic reactions in chemotherapy, and the occurrence of CIPN affects patients' quality of life and can cause interruption of chemotherapy in severe cases, thus reducing the efficacy of chemotherapy. We currently summarize the existing CIPN animal models, including the characteristics of several common animal models such as bortezomibinduced peripheral neuropathy, vincristine-induced peripheral neuropathy, and oxaliplatin-induced peripheral neuropathy. It was found that CIPN may lead to behavioral, histopathological, and neurophysiological changes inducing peripheral neuropathy. However, the mechanism of CIPN has not been fully elucidated, especially the prevention and treatment protocols need to be improved. Therefore, this review article summarizes the progress of research on CIPN animal models and the possible mechanisms and treatment of CIPN.

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“…Long term ER stress activates c-Jun N-terminal kinase (JNK) and p38 MAPK, thereby promoting apoptosis and necrosis (11). In addition, ER stress engages mitochondria in the process of apoptosis through Ca 2+ release (12). Therefore, to achieve effective results, interventions that target ER stress based on apoptosis or oxidative stress need to be developed.…”

Section: Introductionmentioning

confidence: 99%

Compound Qiying Granules Alleviates Diabetic Peripheral Neuropathy by Inhibiting Endoplasmic Reticulum Stress and Apoptosis

Chen

Liang

et al. 2023

Preprint

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Background Diabetic peripheral neuropathy (DPN) is a major complication of diabetes. This study aimed to investigate the therapeutic effects and molecular mechanisms of Compound Qiying Granules (CQYG) for DPN. Methods Rats and RSC96 cells of DPN models were established to evaluate the therapeutic effects of CQYG. Then the morphology and apoptotic changes of sciatic nerves were detected. Further, tandem mass tag based quantitative proteomics technology was used to identify differentially expressed proteins (DEPs) and the underlying molecular mechanisms. Protein expression of key signaling pathways was also detected. Results CQYG treatment significantly improved blood glucose and oxidative stress levels, and further reduced nerve fiber myelination lesions, denervation, and apoptosis in DPN rats. Further, 2176 DEPs were found in CQYG treated DPN rats. Enrichment analysis showed that protein processing in the endoplasmic reticulum (ER), and apoptosis were all inhibited after CQYG treatment. Next, CQYG treatment reduced inflammatory factor expression, mitochondrial damage, and apoptosis in RSC96 cells which induced by high glucose. Transmission electron microscopy results found that CQYG treatment improved the morphology of nerve myelin, mitochondria, and ER. CQYG treatment decreased ER stress and apoptosis pathway proteins that were highly expressed in DPN models. In addition, we also predicted the potential targets of CQYG in DEPs. Conclusions CQYG exerts neuroprotective effects in experimental diabetic neuropathy through anti-ER stress and anti-apoptosis.

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Endoplasmic Reticulum Stress in Chemotherapy-Induced Peripheral Neuropathy: Emerging Role of Phytochemicals

Cited by 6 publications

References 164 publications

Unraveling the Connection: Pain and Endoplasmic Reticulum Stress

Unraveling the Connection: Pain and Endoplasmic Reticulum Stress

Animal models of chemotherapy‐induced peripheral neuropathy for hematological malignancies: A review

Compound Qiying Granules Alleviates Diabetic Peripheral Neuropathy by Inhibiting Endoplasmic Reticulum Stress and Apoptosis

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