Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

This review examines the application of stem cell therapy in myocardial remodeling following myocardial infarction, delving into the complex changes in the cardiac microenvironment after myocardial infarction, the potential mechanisms of stem cell treatment, and the progress of clinical research. It also provides an outlook on future research directions and clinical applications. After myocardial infarction, the heart undergoes a series of complex biological processes, including cardiomyocyte death and hypertrophy, activation and transdifferentiation of fibroblasts, remodeling of the extracellular matrix, functional changes in endothelial cells, and activation of inflammatory responses. These processes ultimately lead to pathological alterations in cardiac structure and function, known as cardiac remodeling. Stem cell therapy and its cell derivatives improve cardiac structure and function through multiple pathways, such as inducing myocardial regeneration, promoting angiogenesis, modulating the inflammatory microenvironment, and reducing fibrosis. However, stem cell therapy still faces many challenges in the treatment of myocardial infarction, such as low cell survival rates, excessive fibrosis, and low clinical translation efficiency. Despite these challenges, stem cell therapy, as an emerging treatment modality, shows great potential in cardiac remodeling after myocardial inf

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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