Suicide transport blockade of motor neuron survival generates a focal graded injury and functional deficit

Liang, Allison; Pagano, Joanna E; Chrzan, Christopher A; McKinnon, Randall D.

doi:10.4103/1673-5374.301032

Cited by 7 publications

(2 citation statements)

References 29 publications

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“…Small-molecule inhibitors targeting this pathway, such as wortmannin and LY294002, which are common PI3K inhibitors, have been studied extensively. Wortmannin binds to the 110 kD catalytic subunit of PI3K, specifically inhibits PI3K, and inhibits the PI3K/Akt signaling pathway [ 31 ]. Wortmannin can also inhibit myosin light chain kinase (MLCK), which is not a specific effect.…”

Section: Discussionmentioning

confidence: 99%

CRTAC1 enhances the chemosensitivity of non-small cell lung cancer to cisplatin by eliciting RyR-mediated calcium release and inhibiting Akt1 expression

Jin,

Zhao,

Chang

et al. 2023

Cell Death Dis

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Sensitivity to platinum-based combination chemotherapy is associated with a favorable prognosis in patients with non-small cell lung cancer (NSCLC). Here, our results obtained from analyses of the Gene Expression Omnibus database of NSCLC patients showed that cartilage acidic protein 1 (CRTAC1) plays a role in the response to platinum-based chemotherapy. Overexpression of CRTAC1 increased sensitivity to cisplatin in vitro, whereas knockdown of CRTAC1 decreased chemosensitivity of NSCLC cells. In vivo mouse experiments showed that CRTAC1 overexpression increased the antitumor effects of cisplatin. CRTAC1 overexpression promoted NFAT transcriptional activation by increasing intracellular Ca2+ levels, thereby inducing its regulated STUB1 mRNA transcription and protein expression, accelerating Akt1 protein degradation and, in turn, enhancing cisplatin-induced apoptosis. Taken together, the present results indicate that CRTAC1 overexpression increases the chemosensitivity of NSCLC to cisplatin treatment by inducing Ca2+-dependent Akt1 degradation and apoptosis, suggesting the potential of CRTAC1 as a biomarker for predicting cisplatin chemosensitivity. Our results further reveal that modulating the expression of CRTAC1 could be a new strategy for increasing the efficacy of cisplatin in chemotherapy of NSCLC patients.

show abstract

Section: Discussionmentioning

confidence: 99%

CRTAC1 enhances the chemosensitivity of non-small cell lung cancer to cisplatin by eliciting RyR-mediated calcium release and inhibiting Akt1 expression

Jin,

Zhao,

Chang

et al. 2023

Cell Death Dis

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show abstract

“…Patients with a facilitatory pro-nociceptive profile may be treated with a drug that reduces facilitation (such as gabapentinoids), while patients with an inhibitory pro-nociceptive profile may be treated with a drug that increases inhibitory capacity; if these findings are confirmed in larger studies (for example, serotonin-noradrenaline reuptake inhibitors). Patients with both a low CPM and a high temporal summation may need a combination of treatments Duloxetine (a selective serotoninnoradrenaline reuptake inhibitor) and tapentadol (a noradrenaline reuptake inhibitor) both restore CPM in patients 55 . Furthermore, when pain is treated, a patient's altered pain modulation profile can be restored to normal, as shown by arthroplasty surgery in osteoarthritis patients; when the diseased joint is replaced, most patients will be pain-free and the central and peripheral processes will return to normal.…”

Section: Mechanisms Of Pain Neuropathic Variationmentioning

confidence: 99%

Untitled

2023

IJPSR

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Neuropathic pain is a chronic illness that originates when abnormal functioning in the nervous system is observed or if the nervous system, including peripheral nerves, spinal cords, and brain, is damaged or not working properly, and originating pain. Therefore, it can be said that neuropathic pain is a chronic illness that directly impacts a large number of patients, society, and healthcare systems all over the world. The prevalence of neuropathic pain is believed to be 7-8% in the general population, and it is supposed to rise in the future. The impact of neuropathic pain on older persons is significant. The medical practitioner faces a problem in reducing neuropathic pain symptoms and improving the patient's quality of life. Older people are easily and badly affected by neuropathic pain and are more susceptible to specific adverse effects. Neuropathic pain is different from nociceptive pain, and there is a requirement for a different treatment strategy for neuropathic pain management. The present review article is based on a detailed literature survey on etiology, symptoms, disease progression, modern approaches to treating neuropathic pain, and the information about marketed drugs used for effective treatment. The recommendations of clinical practices for neuropathic pain are presented in this review and their utility in clinical practice. The outcome-based clinical data research is employed for managing neuropathic pain and mitigating the associated conditions. INTRODUCTION:Neuropathic Pain (NP) is a chronic and complicated pain syndrome that frequently results from tissue damage. Neuropathic Pain is associated with the condition when the nervous system is damaged or not working in a good way. Sometimes, nerve filaments themselves may be damaged and malfunction, resulting in neuropathic pain. Neuropathic pain is caused by a disease or injury to the peripheral or central nervous systems and can strike at any time.

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The skin photoprotective effect of trilinolein: Induction of cellular autophagy via the AMPK-mTOR signaling pathway

Lin,

Deng,

et al. 2024

Toxicology and Applied Pharmacology

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Suicide transport blockade of motor neuron survival generates a focal graded injury and functional deficit

Cited by 7 publications

References 29 publications

CRTAC1 enhances the chemosensitivity of non-small cell lung cancer to cisplatin by eliciting RyR-mediated calcium release and inhibiting Akt1 expression

CRTAC1 enhances the chemosensitivity of non-small cell lung cancer to cisplatin by eliciting RyR-mediated calcium release and inhibiting Akt1 expression

Untitled

The skin photoprotective effect of trilinolein: Induction of cellular autophagy via the AMPK-mTOR signaling pathway

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