COL1A1 and heart failure: Under DOX induction, the expression of Col1a1 and Col5a1 significantly increased, which is a compensatory repair of the body to myocardial injury, aiming to maintain the integrity of the myocardial structure by enhancing collagen deposition [52]; however, the persistent cytotoxicity of DOX will disrupt the compensatory balance, leading to excessive collagen deposition, increasing the stiffness of the ventricular wall and impairing diastolic function [53,54], thereby exacerbating systolic dysfunction and forming a vicious cycle of heart failure progression.