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DOI 10.62347/eoup1787

Медицинская библиотека · American journal of translational research · 2026

Acupuncture-induced HSP70 upregulation in neuroprotection: mitochondrial and anti-apoptotic mechanisms.

Wen Hejun, Tian San, Han Xiao, Xiao Qiuyu, Zhang Hong

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Аннотация

Heat shock protein 70 (HSP70) represents a major stress-inducible chaperone, holding considerable significance in regulating the proteostasis, mitochondrial homeostasis, and apoptosis in the injured nervous system. Acupuncture has shown neuroprotective effects in multiple models of neurological diseases, yet the role of HSP70 as a mechanistic link between acupuncture stimulation and neuronal protection has not been systematically clarified. To this end, current evidence on acupuncture-induced HSP70 regulation is hereby summarized, and its potential contribution to neuroprotection is accordingly discussed, with particular emphasis on mitochondrial preservation and anti-apoptotic signaling. Available studies suggest that acupuncture-associated HSP70 upregulation is linked to enhanced cellular stress adaptation, reduced oxidative injury, stabilization of Bcl-2 family-dependent mitochondrial integrity, inhibition of cytochrome c release and apoptosome formation, and suppression of downstream caspase activation. In addition to these intracellular effects, emerging evidence also uncovers the involvement of HSP70 in neuroinflammatory regulation and neuron-glia communication, suggesting its broader role in shaping the injured neural microenvironment. However, current evidence remains largely associative, leaving several key issues unresolved, including questions of causal necessity, cell-specific regulation, intercellular trafficking, and neuroimmune integration. Overall, HSP70 may represent a promising integrative mediator of acupuncture-induced neuroprotection, yet its precise mechanistic function still warrants further experimental validation.

Для цитирования: Wen Hejun, Tian San, Han Xiao, Xiao Qiuyu, Zhang Hong. Acupuncture-induced HSP70 upregulation in neuroprotection: mitochondrial and anti-apoptotic mechanisms.. American journal of translational research. 2026. DOI: 10.62347/eoup1787.
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