Mechanism of kidney's governance of qi transformation to delay immune senescence through microglial glucose metabolic reprogramming in Alzheimer's disease
|更新时间:2025-06-27
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Mechanism of kidney's governance of qi transformation to delay immune senescence through microglial glucose metabolic reprogramming in Alzheimer's disease
Shanghai Journal of Traditional Chinese MedicineVol. 59, Issue 7, Pages: 51-54(2025)
MIAO Jiarui,ZHAO Danyu,ZHU Zhongkang.Mechanism of kidney's governance of qi transformation to delay immune senescence through microglial glucose metabolic reprogramming in Alzheimer's disease[J].Shanghai Journal of Traditional Chinese Medicine,2025,59(7):51-54.
MIAO Jiarui,ZHAO Danyu,ZHU Zhongkang.Mechanism of kidney's governance of qi transformation to delay immune senescence through microglial glucose metabolic reprogramming in Alzheimer's disease[J].Shanghai Journal of Traditional Chinese Medicine,2025,59(7):51-54. DOI: 10.16305/j.1007-1334.2025.z20240706002.
Mechanism of kidney's governance of qi transformation to delay immune senescence through microglial glucose metabolic reprogramming in Alzheimer's disease
Alzheimer's disease (AD) is believed to begin with kidney deficiency, which leads to dysfunction of kidney's governance of qi transformation, resulting in insufficient nourishment of the brain marrow and functional impairment of brain spirit, thereby initiating the disease. Based on the core pathogenesis axis of "brain marrow-brain spirit" in AD, this paper explores the molecular mechanism by which kidney's governance of qi transformation may influence the microglial glucose metabolic reprogramming in AD to delay immune senescence, with the aim of providing new insights for AD treatment. Glucose metabolic reprogramming-induced immune senescence of microglia is a crucial pathogenic mechanism in AD. The potential molecular mechanism is related to the imbalance of the glucocorticoid-insulin-like growth factor 1 axis. The kidney's governance of qi transformation helps regulate this process, thus delaying immune senescence in microglia.
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