How does tretinoin primarily increase collagen synthesis in the skin?

Tretinoin, a derivative of vitamin A, primarily increases collagen synthesis in the skin through the activation of nuclear gene transcription. This process involves several mechanisms, including the binding of tretinoin to nuclear receptors, specifically retinoic acid receptors (RARs). Once bound, the activated receptors facilitate the transcription of genes that are involved in various skin processes, including collagen production.

Collagen, a key structural protein in the skin, is essential for maintaining skin elasticity and firmness. By promoting the expression of genes that encode collagen and other extracellular matrix components, tretinoin effectively stimulates collagen synthesis, leading to improved skin texture and reduced signs of aging.

While increased sebum production and protection from UVB irradiation are associated with certain benefits of topical retinoids, they do not directly relate to the mechanism through which tretinoin specifically enhances collagen synthesis. Similarly, the displacement of vitamin A from cellular stores does not fundamentally explain how collagen production is increased. Thus, the activation of nuclear gene transcription stands out as the primary and most relevant mechanism.