hsa-mir-4535: The expression of hsa-mir-4535 was found to be elevated in UVB-irradiated skin but significantly suppressed in galangin-treated skin [PMC8714160]. H2O2 was found to enhance hsa-mir-4535 expression and suppress Smad4 RNA expression in HS68 cells [PMC8714160]. The future study will focus on the transcriptional regulation of p53 in the hsa-mir-4535 promoter [PMC8714160]. Galangin was found to restore UVB-induced decrease in collagen formation by repressing hsa-mir-4535 levels and promoting Smad4 signaling in HS68 cells [PMC8714160]. Suppression of hsa-mir-4535 partially restored H2O2-induced collagen impairment in HS68 cells [PMC8714160]. Overexpression of hsa-mir-4535 or inhibition of Smad4 resulted in reduced collagen synthesis under galangin treatment following H2O2 exposure [PMC8714160]. Galangin was found to inhibit hsa-mir-4535 and activate the Smad2/3/4 complex, enhancing collagen synthesis [PMC8714160]. A putative conserved target site for hsa-mir-4535 was predicted on the Smad4 3'-UTR [PMC8714160]. Galangin treatment reversed the trend of hsa-mir-4535 and Smad4 expression, indicating regulation of Smad signaling may be involved in galangin-mediated alleviation of H2O2-induced cell damage [PMC8714160]. Galangin attenuated UVB-induced collagen breakdown by downregulating hsa-mir-4535 targeting Smad4, as shown by qPCR analysis [PMC8714160].\