Platinum-Induced Peripheral Neuropathy (PIPN): ROS-Related Mechanism, Therapeutic Agents, and Nanosystems

Hu, Xi; Jiang, Zhijie; Teng, L.; Yang, Hongyu; Hong, Dongsheng; Zheng, Dongsheng; Zhao, Qingwei

doi:10.3389/fmolb.2021.770808

Cited by 10 publications

(6 citation statements)

References 108 publications

(125 reference statements)

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“…The current author proposes that primary afferent peripheral terminal hyperexcitation with “leakiness” at Piezo2 is such a pathological condition in DOMS. Accordingly, it is not surprising that platinum-analogue drugs also elevate ROS production as the primary mechanism of platinum-induced peripheral neuropathy [ 110 ] with the activation of the NF-kappa B pathway [ 111 ].…”

Section: Oxidative Stress and Redox Imbalancementioning

confidence: 99%

Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation

Sonkodi

2022

Biomolecules

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Piezo2 transmembrane excitatory mechanosensitive ion channels were identified as the principal mechanotransduction channels for proprioception. Recently, it was postulated that Piezo2 channels could be acutely microdamaged on an autologous basis at proprioceptive Type Ia terminals in a cognitive demand-induced acute stress response time window when unaccustomed or strenuous eccentric contractions are executed. One consequence of this proposed transient Piezo2 microinjury could be a VGLUT1/Ia synaptic disconnection on motoneurons, as we can learn from platinum-analogue chemotherapy. A secondary, harsher injury phase with the involvement of polymodal Aδ and nociceptive C-fibers could follow the primary impairment of proprioception of delayed onset muscle soreness. Repetitive reinjury of these channels in the form of repeated bout effects is proposed to be the tertiary injury phase. Notably, the use of proprioception is associated with motor learning and memory. The impairment of the monosynaptic static phase firing sensory encoding of the affected stretch reflex could be the immediate consequence of the proposed Piezo2 microdamage leading to impaired proprioception, exaggerated contractions and reduced range of motion. These transient Piezo2 channelopathies in the primary afferent terminals could constitute the critical gateway to the pathophysiology of delayed onset muscle soreness. Correspondingly, fatiguing eccentric contraction-based pathological hyperexcitation of the Type Ia afferents induces reactive oxygen species production-associated neuroinflammation and neuronal activation in the spinal cord of delayed onset muscle soreness.

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Section: Oxidative Stress and Redox Imbalancementioning

confidence: 99%

Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation

Sonkodi

2022

Biomolecules

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“…Excessive ROS generation induced by platinum agents such as oxaliplatin, that leads to oxidative stress and mitochondrial dysfunction, contribute to the development of CIPN. 45,76 DRG neurons exposed to oxaliplatin in vitro induced a dose-dependent and time-dependent mitochondrial production of ROS. 50,63 Given the observed enrichment of ETC components following MTM rescue, we investigated whether DRG neurons increased their content of ROS in response to oxaliplatin treatment in vivo and if MTM treatment could reverse this effect.…”

Section: Resultsmentioning

confidence: 94%

“…Platinum-based chemotherapy agents like cisplatin and oxaliplatin accumulate and form DNA adducts in DRG that induce DNA/ mitochondrial damage, enhancing reactive oxygen species (ROS) production while activating nociceptor-associated channels. 45,63,76,102 Exactly how oxaliplatin or other platinum chemotherapy increase mitochondrial ROS is poorly understood. Nevertheless, increased mitochondrial ROS levels are associated with cisplatin's and oxaliplatin's neurotoxicity in painful CIPN.…”

Section: Mitochondria and Mithramycinmentioning

confidence: 99%

Chemotherapy for pain: reversing inflammatory and neuropathic pain with the anticancer agent mithramycin A

Lee

Sheehan

et al. 2023

Pain

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“…In line with the aforementioned, platinum analogue chemotherapeutic drug-induced ROS production contributes to peripheral neuropathy [ 118 ], with NF-κB pathway activation [ 119 ]. The ROS derived NF-κB activation may also have a role in muscle cells as well, with associated NGF upregulation on them [ 120 ].…”

Section: Agingmentioning

confidence: 99%

Miswired Proprioception in Amyotrophic Lateral Sclerosis in Relation to Pain Sensation (and in Delayed Onset Muscle Soreness)—Is Piezo2 Channelopathy a Principal Transcription Activator in Proprioceptive Terminals Besides Being the Potential Primary Damage?

Sonkodi

2023

Life

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Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative multisystem disease, with an unknown pathomechanism, resulting in progressive motoneuron loss. In 90–95% of cases, ALS is sporadic, but close to 10% of ALS is familial with inherited gene mutations from family members. Recently, a non-contact dying-back injury mechanism theory of ALS postulated that irreversible intrafusal proprioceptive terminal degeneration induces the non-resolving progressive impairment of the proprioceptive circuitry, leading to motoneuron loss, progressive overloading and depletion of the central nervous system, and eventually to death. The current manuscript proposes that irreversible Piezo2 channelopathy of this proprioceptive terminal degeneration induces constantly activated and dysregulated transcription process in ALS, providing access to underlying pathogenic gene variants and letting the cell-type-specific noncoding DNA mutations become more apparent. This opinion piece proposes that ALS genes are associated with the Piezo2 channelopathy mechanism both downstream and upstream, and their mutations, along with the aging process, could explain the non-contact dying-back injury mechanism theory of ALS. Moreover, irreversible microinjury of the Piezo2 ion channel could be the primary damage or the root cause of death in ALS. Finally, the current manuscript also depicts the pathomechanism as to why ALS is considered a painless disease.

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Platinum-Induced Peripheral Neuropathy (PIPN): ROS-Related Mechanism, Therapeutic Agents, and Nanosystems

Cited by 10 publications

References 108 publications

Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation

Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation

Chemotherapy for pain: reversing inflammatory and neuropathic pain with the anticancer agent mithramycin A

Miswired Proprioception in Amyotrophic Lateral Sclerosis in Relation to Pain Sensation (and in Delayed Onset Muscle Soreness)—Is Piezo2 Channelopathy a Principal Transcription Activator in Proprioceptive Terminals Besides Being the Potential Primary Damage?

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