Similar to fullerenes, carbon nanotubes and graphene, carbon dots (CDs) are causing a lot of research work in their own right. CDs are a type of surface-passivated quantum dot that contain carbon atoms. Their distinctive characteristics, such as luminescent emission that varies with size and wavelength, resistance to photobleaching, easy biological binding, lack of toxicity, and economical production without the need for intricate synthetic processes, have led to a noteworthy surge in attention within the research community. Different techniques can be utilized to create these CDs, spanning from basic candle burning to laser ablation. This review article delves into the principles of fluorescence technology, providing insights into how different synthesis methods of quantum dots impact their luminescent properties. Additionally, it highlights the latest applications of quantum dots in catalysis and biomedical fields, with special emphasis on the current status of luminescent properties in biology and chemistry. Towards the end, the article discusses the limitations of quantum dots in current practical applications, pointing out that CDs hold promising potential for future applications.

The delay in wound healing caused by chronic wounds or pathological scars is a pressing issue in clinical practice, imposing significant economic and psychological burdens on patients. In particular, with the aging of the population and the increasing incidence of diseases such as diabetes, impaired wound healing is one of the growing health problems. MicroRNA (miRNA) plays a crucial role in wound healing and regulates various biological processes. Our results show that miR–618 was significantly upregulated during the inflammatory phase of wound healing.Subsequently, miR–618 promotes the secretion of pro–inflammatory cytokines and regulates the proliferation and migration of keratinocytes. Mechanistically, miR–618 binds to the target gene–Atp11b and inhibits the PI3K–Akt signaling pathway, inhibiting the epithelial–mesenchymal transition (EMT) of keratinocytes. In addition, the PI3K–Akt signaling pathway induces the enrichment of nuclear miR–618, and miR–618 binds to the promoter of Lin7a to regulate gene transcription. Intradermal injection of miR–618 antagomir around full–thickness wounds in peridermal mice effectively accelerates wound closure compared to control. In conclusion, miR–618 antagomir can be a potential therapeutic agent for wound healing.