New Elastic Fiber Formation Can Be Induced by Intradermal Injection of Transparent Porcine‐Derived Type I Atelocollagen in Mice

Background Skin aging is characterized by the loss of collagen and elastic fibers, leading to reduced elasticity and wrinkle formation. Although skin boosters are widely used for skin rejuvenation, direct evidence of elastic fiber regeneration remains limited. Aims To evaluate the regenerative effects of transparent porcine‐derived low‐immunogenic Type I atelocollagen in naturally aged skin. Methods Transparent porcine‐derived Type I atelocollagen was injected intradermally into the dorsal skin of young (4 months old) and naturally aged (15 months old) mice. Skin tissues were collected 2 and 4 weeks after treatment. Histological analyses (hematoxylin and eosin and Verhoeff staining) were performed to assess skin thickness and elastic fiber regeneration. Macrophage polarization was evaluated by immunohistochemistry, enzyme‐linked immunosorbent assay, and quantitative real‐time PCR. The expression of elastogenesis‐related genes (Eln, Ebp, Fbn1, Fbln5, Lox, Loxl1, Mfap4, and Ltbp4) and skin elasticity in aged mice were also analyzed. Results Transparent porcine‐derived Type I atelocollagen significantly increased epidermal and dermal thickness and promoted robust elastic fiber regeneration. Newly formed elastic fibers extended into the upper dermis, restoring a dermal architecture resembling that of young skin. Transient activation of the M2 macrophage pathway was observed during tissue remodeling, with no histological evidence of persistent inflammation at 4 weeks after treatment. Conclusions Transparent porcine‐derived Type I atelocollagen enhanced skin thickness, promoted elastic fiber regeneration, and restored youthful dermal architecture while demonstrating favorable biocompatibility through transient M2 macrophage‐mediated tissue remodeling. These findings support the potential of transparent porcine‐derived atelocollagen as an effective skin booster for skin rejuvenation, warranting further investigation of its molecular mechanisms and long‐term clinical efficacy.