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[Progress of researches on acupuncture treatment of diseases by regulating endoplasmic reticulum stress].

[Progress of researches on acupuncture treatment of diseases by regulating endoplasmic reticulum stress].

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Original abstract

Endoplasmic reticulum stress (ERS) is one of the major defense networks in mammals, but continuous ERS will lead to cell apoptosis, inducing initiation and progression of many human diseases. Biochemical, physiological and pathological stimuli induced ERS may help the cells adapt to and survive stress conditions by activating unfolded protein response (UPR), ER-overload response and sterol modulation cascade reaction. Abundant outcomes of clinical and experimental studies in recent 5 years showed that acupuncture and moxibustion therapies are effective in improving some symptoms of nervous system diseases as stroke, Parkinson's disease, convulsion, cardiovascular diseases, diabetes mellitus, non-alcoholic fatty liver disease, spinal cord injury, muscular injury, etc., which is closely associated with their functions in relieving excessive ERS and cell apoptosis via modulating UPR pathway. Some important molecules or signaling pathways such as glucose-regulated protein 78(GRP78), Caspase-12, ER transmembrane kinase inositol-requiring and ER-to-nucleus signaling protein (IRE1P), phosphorylated extracellular signal-regulated kinase (p-ERK)/eukaryotic translation initiation factor 2α(eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein (CHOP), etc. have been demonstrated to be involved in the effects of acupuncture-moxibustion interventions. But, the mechanism of acupuncture-moxibustion underlying improvement of ERS remains far more unclear. Future studies targeting the combination of molecules and holistic function, verification of changes of the involved protein molecules and multiple signaling pathways, balancing regulation between the cell survival and apoptosis, etc. by adopting syndrome-differentiation-based acupoints are definitely needed.

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