Materials today. BioSep 14, 2026

Relieving nerve pain by using tiny particles that deliver working mitochondria and a mitochondria-cleanup booster to reshape cell energy centers

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 15, 2026

Abstract

Significant deficits in mitochondrial quantity and quality were found in dorsal root ganglion neurons and satellite glial cells from a chemotherapy-induced peripheral neuropathy model.

Mitochondrial dysfunction is identified as a key factor in neuropathic pain.
An extracellular vesicle-based platform (EVs@Mi/UR) was developed to enhance mitochondrial function.
EVs@Mi/UR increased mitochondrial mass in dorsal root ganglion neurons and satellite glial cells through mitochondrial transplantation.
The platform improved mitochondrial quality by removing damaged organelles, leading to better mitochondrial respiration and metabolic function.
In mouse models of chemotherapy-induced peripheral neuropathy and spared nerve injury, EVs@Mi/UR reduced pain sensitivity significantly.
Even without baseline mitochondrial deficits, EVs@Mi/UR demonstrated analgesic effects by enhancing mitochondrial quality.

Simplified

Neuropathic pain remains a major clinical challenge due to limited efficacy and tolerability of current treatments. Mitochondrial dysfunction in dorsal root ganglion (DRG) cells is recognized as a key pathogenic mechanism, but effective strategies to restore mitochondrial homeostasis are lacking. Here, we first identified profound deficits in mitochondrial quantity and quality in DRG neurons and satellite glial cells (SGCs) from a chemotherapy-induced peripheral neuropathy (CIPN) model. To address this, we developed an extracellular vesicle-based nanoplatform (EVs@Mi/UR) loaded with a mitophagy inducer, which integrates exogenous mitochondrial transplantation with mitophagy induction. EVs@Mi/UR not only increased mitochondrial mass in DRG neurons and SGCs through efficient mitochondrial transplantation, but also improved mitochondrial quality by eliminating damaged organelles, thereby enhancing mitochondrial respiration and metabolic function. In both CIPN and spared nerve injury (SNI) mouse models, EVs@Mi/UR significantly alleviated mechanical allodynia, thermal hyperalgesia, and cold hypersensitivity with superior efficacy. Notably, even in SNI models that did not exhibit baseline mitochondrial deficits, EVs@Mi/UR still produced analgesic effects by improving mitochondrial quality. This work establishes mitochondrial remodeling as a promising strategy for neuropathic pain and provides a translatable EV-based nanoplatform for dual-modality mitochondrial intervention.

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Relieving nerve pain by using tiny particles that deliver working mitochondria and a mitochondria-cleanup booster to reshape cell energy centers

Abstract

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