Macrophage-secreted lactate directly activates fibroblast scarring through MCT1 transporters and histone lactylation, revealing a metabolite-driven epigenetic pathway for hypertrophic scar development. The mechanism involves lactate crossing cellular membranes to modify chromatin proteins, switching on profibrotic gene expression programs that drive excessive collagen deposition. This metabolic-epigenetic axis represents a fundamental shift from viewing scars as purely mechanical tissue responses to understanding them as metabolically programmed cellular states. The discovery positions lactate as both an inflammatory signal and direct epigenetic modifier, suggesting why some individuals develop problematic scarring while others heal cleanly. Unlike previous research focusing on growth factors or mechanical tension, this work identifies a targetable small-molecule pathway. Potential therapeutic interventions could include MCT1 inhibitors to block lactate uptake or compounds that prevent histone lactylation without disrupting normal wound healing. The findings may extend beyond dermatology to other fibrotic diseases where macrophage activation and abnormal healing intersect, including pulmonary fibrosis and cardiac remodeling. However, translation requires careful validation since lactate serves essential roles in normal tissue repair and energy metabolism.