Various growth factors are key molecules in wound healing and exert regulatory effects at all stages of healing. Fibroblast growth factors (FGFs), with their prominent pro-growth activity, play a crucial role in promoting proliferation during the proliferative phase of wound healing. By binding to fibroblast growth factor receptors, FGFs activate downstream signaling pathways to regulate wound inflammation, reduce oxidative stress, promote cell proliferation, angiogenesis, and extracellular matrix remodeling. This facilitates the transition of wounds from the " inflammatory phase" to the " proliferative phase" and enhances proliferative healing. The clinical therapeutic value of FGFs in acute and chronic wounds has been widely confirmed, but their full efficacy is limited by issues such as short half-life and poor delivery efficiency. Research focusing on innovative FGF delivery materials and molecular modification strategies will become a key direction to break through current therapeutic bottlenecks and unlock their greater therapeutic potential.

Various growth factors are key molecules in wound healing and exert regulatory effects at all stages of healing. Fibroblast growth factors (FGFs), with their prominent pro-growth activity, play a crucial role in promoting proliferation during the proliferative phase of wound healing. By binding to fibroblast growth factor receptors, FGFs activate downstream signaling pathways to regulate wound inflammation, reduce oxidative stress, promote cell proliferation, angiogenesis, and extracellular matrix remodeling. This facilitates the transition of wounds from the " inflammatory phase" to the " proliferative phase" and enhances proliferative healing. The clinical therapeutic value of FGFs in acute and chronic wounds has been widely confirmed, but their full efficacy is limited by issues such as short half-life and poor delivery efficiency. Research focusing on innovative FGF delivery materials and molecular modification strategies will become a key direction to break through current therapeutic bottlenecks and unlock their greater therapeutic potential.

Cystic echinococcosis (CE) is a zoonotic infection caused by Echinococcus granulosus larvae. It seriously affects the development of animal husbandry and endangers human health. Due to a poor understanding of the cystic fluid formation pathway, there is currently a lack of innovative methods for the prevention and treatment of CE. In this study, the protoscoleces (PSCs) in the encystation process were analyzed by high-throughput RNA sequencing. A total of 32,401 transcripts and 14,903 cDNAs revealed numbers of new genes and transcripts, stage-specific genes, and differently expressed genes. Genes encoding proteins involved in signaling pathways, such as putative G-protein coupled receptor, tyrosine kinases, and serine/threonine protein kinase, were predominantly up-regulated during the encystation process. Antioxidant enzymes included cytochrome c oxidase, thioredoxin glutathione, and glutathione peroxidase were a high expression level. Intriguingly, KEGG enrichment suggested that differentially up-regulated genes involved in the vasopressin-regulated water reabsorption metabolic pathway may play important roles in the transport of proteins, carbohydrates, and other substances. These results provide valuable information on the mechanism of cystic fluid production during the encystation process, and provide a basis for further studies on the molecular mechanisms of growth and development of PSCs.