Research progress of STAT3 in atrial fibrosis

Atrial fibrosis refers to the abnormal proliferation and deposition of collagen fibers in the atrial muscle interstitium, resulting in changes in the extracellular matrix of the atrial muscle. Normally, fibrous tissue accounts for 2% - 4% of the atrial tissue content, but in the case of atrial fibrosis, the collagen fibrous tissue content may exceed 10% of the atrial tissue. Atrial fibrosis is a serious hazard to heart health. On the one hand, it accelerates the occurrence and maintenance of atrial fibrillation, making the condition more complex, and on the other hand, atrial fibrosis leads to changes in the structure of the atrium, increasing the risk of complications of heart disease, such as heart failure and cardiac arrest, etc. Therefore, it is of great significance to study the pathogenesis of atrial fibrosis and find new fibrosis-related signaling pathways for the prevention and treatment of cardiovascular diseases. Signal transducer and activator of transcription 3 (STAT3) is a protein that belongs to the signal transduction and activation domain family. STAT3 plays an important role in cell signaling and can regulate the expression of a variety of genes, thereby affecting the biological functions of cells such as growth, differentiation and migration. In recent years, studies have found that STAT3 also plays an important role in the occurrence and progression of atrial fibrosis. This article will review the research on the role of STAT3 in atrial fibrosis.