Cellular senescence is accompanied by mitochondrial dysfunction and decline in type I collagen production, contributing to age-related tissue deterioration. However, the post-transcriptional mechanisms underlying senescence-associated collagen decline remain poorly understood. Here, we investigated the effects of chlorella hot water extract (CHWE) on mitochondrial function and collagen production in senescent human fibroblasts. CHWE restored mitochondrial membrane potential, ATP production, and redox balance through upregulation of SOD2. Notably, CHWE increased collagen protein levels without altering COL1A1 mRNA, indicating post-transcriptional regulation. miRNA profiling across young, senescent, and CHWE-treated senescent fibroblasts revealed that miR-193a-5p was upregulated during senescence (1.73-fold) and normalized by CHWE treatment. Functional validation confirmed that miR-193a-5p mimic suppressed COL1A1 protein. These findings identify a senescence-miR-193a-5p-COL1A1 axis in which age-dependent miR-193a-5p accumulation represses collagen translation, and CHWE reverses this process. By simultaneously restoring mitochondrial bioenergetic capacity and relieving miRNA-mediated translational repression, CHWE promotes efficient collagen recovery in senescent cells through complementary mechanisms. This study reveals a translational regulatory mechanism of collagen decline during cellular aging and highlights CHWE as a functional food supplement and a potential multi-target agent for age-related tissue deterioration.
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