COL1A2 and cardiac hypertrophy: Lastly, gene expression analysis demonstrated that the molecular fingerprint of pathological cardiac hypertrophy was partly reversed by α-MSH with a significant reduction in TAC-induced expression of fibrosis-related genes including Col1a2 (collagen type I, alpha 2) and Mmp2 (matrix metalloproteinase-2) (Appendix Fig. S1).