Atrial fibrillation is considered the most common heart disease worldwide, and the prevalence has increased by 30% over the past 20 years. With the aging of the world’s population and the continuous improvement of chronic disease treatment, it is predicted that the proportion of morbidity and incidence of atrial fibrillation will continue to rise in the next 20 years, which undoubtedly brings great pressure to the society and economy [1] . Atrial remodeling is a central step in the development and progression of AF, which can be divided into electrical, structural, and autonomic aspects. Atrial fibrosis refers to the abnormal activity, growth and differentiation of fibroblasts, accompanied by excessive accumulation and production of myocardial extracellular matrix (ECM) proteins [2] . A significant pathological change of atrial fibrillation is atrial fibrosis, which is closely related to the abnormal structure and function of the heart. This process involves the electronic and structural reconstruction of atrial fibrillation, which is also the core step of atrial fibrillation. With the deepening of atrial fibrosis, the electrical characteristics of the atrium can be changed, which further increases the possibility of recurrence of atrial fibrillation. Therefore, early identification and intervention of atrial fibrosis, especially in the diagnosis and treatment of atrial fibrillation, plays a vital role in the control of the disease. According to scientific research, miRNA can affect cardiac remodeling by affecting the expression of ion channel proteins and adjusting the decomposition balance of extracellular matrix, which further demonstrates its function of accelerating and resisting atrial fibrillation. The stability and tissue specificity of miRNA make it play an important role in the study of atrial fibrosis in atrial fibrillation. Therefore, the in-depth exploration of the association between miRNA and atrial fibrosis in atrial fibrillation will provide a powerful starting point for the discovery of new prevention and treatment goals of atrial fibrillation, and provide a reference for future biomarkers and diagnostic work. To provide a new therapeutic approach to further improve the recurrence of atrial fibrillation after radiofrequency ablation [3] - [7] .

The occurrence of atrial fibrillation is the combined effect of many factors, and its core feature is the disorder of atrial electrical activity. Relevant studies have confirmed that the electrical and pathological mechanisms of atrial fibrillation have been widely recognized. The development and maintenance of atrial fibrillation can not be separated from stimulating substances. Most of the stimulating elements are produced by abnormal discharges at the ostium of the pulmonary veins, which are often caused by changes in calcium homeostasis or autonomic activity. It can stimulate a series of behaviors including early afterdepolarization and delayed afterdepolarization, and these abnormal discharges can induce atrial fibrillation by cardiac electrical stimulation [8] - [13] . The origin of atrial fibrillation is atrial stroma. In particular, left atrial structural remodeling and atrial interstitial fibrosis are considered to be the main causes of arrhythmias. This has been demonstrated in many animal models of atrial fibrosis, which may lead to local conduction disorders and block, thereby increasing the risk of reentry into the circuit, which also increases the sensitivity to atrial fibrillation. In patients with lone paroxysmal atrial fibrillation, the normal heart panorama may show extensive or patchy fibrosis. Atrial tachycardia may also cause ECM accumulation. Cardiac fibrosis is the cause and result of atrial fibrillation [14] .

According to the theory of histopathology, atrial myocardial fibrosis can be divided into three types: reparative fibrosis, reactive fibrosis and perivascular tissue fibrosis. Reparative fibrosis is the replacement of dead cardiomyocytes by extracellular matrix and fibrotic fibroblasts, which affects the structure of myocardial bundles and also disrupts the transmission of electrical current. Reactive fibrosis is due to the abnormal accumulation of extracellular matrix caused by the expansion of the endomysium and perimuscular tissue, while perivascular fibrosis is due to the expansion of the microvascular adventitia. Both types of fibrosis may be the product of a long-term fibrotic stimulus that does not completely alter the architecture of the cardiac fascicles [15] . Reactive and reparative fibrosis may coexist in the left ventricle in patients with atrial fibrillation. The essence of fibrosis is the accumulation and change of ECM, and the core link of this process is to awaken the fibroblasts in the myocardium and make them become myofibroblasts. The function of myofibroblasts is to increase the accumulation of ECM and reduce the decomposition of ECM, thus causing fibrosis. ECM is a non-cellular component of the heart, which contains a variety of matrix proteins. Among these proteins, the content of proprotein is the highest in all proteins, and it accounts for 80% of the total ECM. Within these categories, the collagen content of types I and III is the most closely associated with fibrosis. The occurrence of fibrosis is triggered by a variety of factors and produce interactive effects. At the same time, atrial fibrillation itself can also trigger a variety of signal transduction pathways involved in the formation of cardiac fibrosis. Current scientific findings suggest that the main drivers of cardiac fibrosis are the renin-angiotensin-aldosterone system (RAAS), PI3K/Akt, and MAPK signaling pathways. And the signal transduction pathway of nuclear transcription factor-κB. The central mediators of atrial fibrillation include inflammation and oxidative stress, which can exacerbate cardiac remodeling and promote the occurrence of atrial fibrillation. After the heart is damaged, the number of inflammatory signaling molecules rises sharply, among which monocytes and macrophages are the main sources of inflammatory factors, and they produce a large number of pro-inflammatory substances. These inflammatory cytokines are capable of co-acting with the previously described means of stimulating fibrosis [16] .

The existence of atrial fibrillation can promote atrial remodeling, lead to and maintain the occurrence and progress of atrial fibrillation, forming a vicious circle. Therefore, early diagnosis and intervention of atrial fibrosis is the key to reduce the recurrence of atrial fibrillation. The main impact indicators are as follows:

With the aging of the population in China becoming more and more serious, the proportion of morbidity with atrial fibrillation is increasing every year. Catheter ablation of atrial fibrillation has become the main treatment for patients with atrial fibrillation, but the risk of recurrence is also increasing [22] . In the early phase of AF, left atrial remodeling is mainly reflected in the changes of electrophysiology and ion channels, which is called electrical remodeling. Then, with the development of time, it will lead to fibrosis of atrial muscle and extracellular matrix, amyloid changes, cell death and other structural changes, resulting in structural remodeling, and finally lead to interstitial fibrosis and left atrial expansion. Therefore, it is critical to effectively identify the severity of left atrial fibrosis, while working to minimize the recurrence of AF after catheter ablation, so as to minimize its recurrence [23] . The expression of miRNA has obvious tissue or cell specificity in vivo, can stably exist in serum or plasma, and can be easily obtained. Therefore, miRNA may become a new biomarker of AF, which can help to evaluate the risk and treatment effect of AF. In addition, miRNA may be a therapeutic target for atrial fibrillation. However, due to the wide spectrum of genes and miRNAs involved in AF fibrosis, and the precise and complex regulation of miRNAs, the exploration of such biological regulatory networks has not yet reached sufficient depth and integrity. Therefore, how to manage the side effects of miRNA on multiple targets, that is, to enhance the targeting specificity of miRNA, is a research problem that needs to be urgently dealt with. We firmly believe that with the comprehensive, systematic and in-depth study of miRNAs related to AF, the ideal of preventing, reversing and treating AF through precise regulation of miRNAs will eventually become a reality [24] . Therefore, it is necessary to explore the mechanism of atrial fibrillation more deeply. Accurate prediction of the various effects that may cause AF recurrence after surgery will identify potential risks early in the actual medical procedure and implement necessary protective strategies.