Skin aging is closely related to mitochondrial dysfunction and cell cycle abnormalities, and developing intervention strategies targeting mitochondrial quality control is an important direction for anti-aging research. In this study, we investigated the anti-aging mechanism of Camellia japonica flower (CJF) extract and its active ingredient hyperoside based on a doxorubicin (DOX)-induced endogenous senescence model in human skin fibroblasts (HSFs). LC-MS proteomics analysis revealed that CJF extract and hyperoside specifically activated the FUNDC1-mediated mitochondrial autophagy pathway, significantly ameliorated the DOX-induced decrease in mitochondrial membrane potential and the accumulation of reactive oxygen species (ROS), and alleviated the cellular S-phase blockade and reversed the high expression of senescence-associated β-galactosidase (SA-β-gal). Further studies showed that the two cleared damaged mitochondria by enhancing mitochondrial autophagy and restoring cellular energy metabolism homeostasis while promoting type III collagen and elastin synthesis and repairing the expression of Claudin 1 related to skin barrier function. For the first time, the present study reveals the molecular mechanism of CJF extract in delaying skin aging by regulating the FUNDC1-dependent mitochondrial autophagy pathway, which provides a theoretical basis and a candidate strategy for developing novel anti-aging agents targeting mitochondrial quality control.

Camellia japonica L. (Theaceae) seed oil is an essential component for skin protection, attributed to its antioxidant properties and anti-aging effects. In this study, Camellia japonica seed oil underwent fermentation with Sporidiobolus pararoseus (Fell & Tallman, CGMCC No. 39106, commercial name: Longevity yeast of 1021-year-Camellia japonica). The post-fermented oil, designated Longevity Yeast Oil (LYO), was used in the present research. Gas chromatography–mass spectrometry analysis demonstrated that methyl esterification of LYO afforded twelve fatty acid methyl esters. We used an aging model in human epidermal keratinocytes and human skin fibroblasts exposed to ultraviolet B (UVB) to explore the anti-skin aging effects and mechanisms of LYO. The results of the CCK-8 assay demonstrated that LYO exhibited no cytotoxicity but instead displayed potential proliferative activity, indicating its excellent safety profile. Quantitative real-time polymerase chain reaction analyses confirmed that LYO downregulated the expression of autophagy marker p62 and upregulated LC3B, thereby activating the autophagic pathway. Further investigation revealed that LYO protected against UVB-induced apoptosis, promoted the synthesis of collagen and elastin, and upregulated the expression of loricrin, filaggrin, and ceramides, effectively reversing UVB-induced skin cellular aging. Notably, we further revealed that LYO alleviated UVB-induced cutaneous photoaging via activating cellular autophagy pathway. In conclusion, LYO demonstrated biocompatibility and conferred protection to skin cells against photoaging, thereby establishing a theoretical basis for the development of innovative autophagy-targeted anti-aging therapies.