Autophagy: A Key Link Between Antioxidant Processes and Oral Tissue Regeneration

Enhancing autophagy can restore redox homeostasis and promote multiple oral tissue regeneration. The natural antioxidant genistein has been found to protect against alveolar bone loss and periodontal tissue degradation in mouse periodontitis induced by LPS, by up-regulating autophagy and inhibiting mitochondrial oxidative damage [74]. Similar results have been observed in human PDLSC [75]. Resveratrol has been found to inhibit autophagy-JNK signaling cascade and suppress TNF-α-induced inflammation in human DPSCs [76]. Additionally, the participation of NRF2 and its target antioxidant response is crucial in maintaining cellular redox homeostasis in both periodontitis and oral squamous cell carcinoma [77],[78]. NRF2 has been shown to be involved in BMSC-mediated oxidative damage repairment in t-BHP-damaged neurons [79], and the Keap1/Nrf2/HO-1 pathway has been implicated in regulating proliferation and viability of h-PDLSCs in diabetic patients [80].

Overall, the research in this field indicates that autophagy is a crucial player in the crosstalk between antioxidant processes and oral tissue regeneration. However, the precise role of ROS/RNS triggered or inhibited by autophagy in stem cells warrants further investigation, particularly in the context of oral tissue regeneration. Furthermore, it is essential to elucidate how to balance stem cell survival and apoptosis/death via autophagy regulation.