Mechanical properties of the extracellular matrix directly influence cellular identity transitions during teleost fish heart development, with stiffer environments promoting cardiomyocyte differentiation while softer matrices favor endothelial cell formation. This mechanobiology mechanism operates independently of traditional genetic signaling pathways, suggesting physical forces serve as fundamental drivers of evolutionary innovation. The findings illuminate how biomechanical constraints could shape organ architecture across vertebrate lineages, potentially explaining why certain cardiac structures emerged repeatedly in fish evolution. For regenerative medicine, this work indicates that manipulating substrate stiffness might control stem cell differentiation more precisely than chemical factors alone. The research bridges developmental biology with evolutionary theory, demonstrating that physical properties of tissues can generate phenotypic diversity without requiring new genetic mutations. However, the study's focus on fish hearts limits direct translation to mammalian cardiac regeneration, and the molecular mechanisms linking mechanical stress to transcriptional programs remain incompletely characterized. This represents a paradigm shift toward viewing evolution through a biophysics lens rather than purely genetic terms.