Autophagy plays a crucial role in the physiopathological mechanisms of diseases by regulating cellular functions and maintaining cellular homeostasis, which has garnered extensive attention from researchers worldwide. The holistic regulation and bidirectional regulation effects of acupuncture can modulate cellular autophagy, promoting or restoring the homeostasis of the body’s internal environment to achieve therapeutic outcomes. This paper systematically reviews the research progress on the use of acupuncture for treating various diseases via the autophagy pathway, summarizes signal pathways related to acupuncture regulating autophagy, and analyzes the deficiencies present in the existing research. The review results indicate that the mechanism of action of acupuncture on autophagy dysfunction is reflected in the changes in LC3, Beclin1, p53, and autophagy-associated (ATG) protein expression, and regulates signaling pathways and key proteins or genes. The regulatory effect of acupuncture on autophagy capacity is bidirectional: it inhibits the abnormal activation of autophagy to prevent exacerbation of injury and reduce apoptosis, while also activating or enhancing autophagy to promote the elimination of inflammation and reduce oxidative stress. Further analysis suggests that the mechanisms of acupuncture regulating autophagy are insufficiently explored. Future research should prioritize the development of more appropriate animal models, analyzing the accuracy of relevant pathways and the specificity of indicators, exploring the synergistic effects among targets and signaling pathways, clarifying the regulatory mechanisms of acupuncture at various stages of autophagy, and evaluating the efficacy of acupuncture in autophagy modulating. This paper offers valuable insights into the regulation of autophagy by acupuncture.

Most patients with irritable bowel syndrome have diarrhea or constipation, two opposite bowel habits. Although defecation habits represent opposing phenotypes, patients across all subtypes exhibit visceral hypersensitivity. This review explores the common pathway that causes visceral hypersensitivity: the mast cell–PAR2–TRP axis. The mechanism involves tryptase released by mast cells. Furthermore, tryptase activates PAR2, which sensitizes downstream TRP ion channels that conduct pain signals. The review also examines the factors leading to the formation of different fecal characteristics. In terms of treatment, this review also summarizes therapeutic agents targeting different components of this axis. Future pharmaceutical research should focus more on the mast cell–PAR2–TRP axis.