Cardiac fibrosis, a condition characterized by the deposition of excess collagen in the cardiac tissue, is a major complication of various cardiovascular diseases, including myocardial infarction, hypertension, and different types of cardiomyopathies. CAR T-cell therapy, a form of immunotherapy that involves the genetic modification of T cells to recognize and target specific antigens, has shown promise in the treatment of various cancers and autoimmune diseases. The rationale behind using CAR T-cell therapy to treat cardiac fibrosis lies in the fact that fibrosis is often driven by the activation of pro-fibrotic immune cells, such as myofibroblasts. By targeting these pro-fibrotic cells with CAR T-cells, it may be possible to reduce the severity of cardiac fibrosis. Enhancing CAR T-cell therapy through innovative nanoparticle delivery systems provides a comprehensive approach to treating cardiac fibrosis, with experimental evidence indicating potential in reducing fibrosis and improving cardiac function. Despite these benefits, significant challenges such as cardiotoxicity and cardiovascular complications remain. Therefore, this review explores the molecular mechanisms underlying cardiac fibrosis and the effects of CAR T-cell therapy on the heart, elucidating both its antifibrotic properties and associated cardiotoxic effects based on findings from recent studies.