Abstract
Myocardial fibrosis is characterized by excessive deposition of myocardial interstitial collagen, abnormal distribution, and excessive proliferation of fibroblasts. According to the researches in recent years, myocardial fibrosis, as the pathological basis of various cardiovascular diseases, has been proven to be a core determinant in ventricular remodeling. Pressure load is one of the causes of myocardial fibrosis. In experimental models of pressure-overload-induced myocardial fibrosis, significant increase in left ventricular parameters such as interventricular septal thickness and left ventricular posterior wall thickness and the decrease of ejection fraction are some of the manifestations of cardiac damage. These morphological and functional changes have a serious impact on the maintenance of physiological functions. Therefore, establishing a suitable myocardial fibrosis model is the basis of its pathogenesis research. This paper will discuss the methods of establishing myocardial fibrosis model and compare the advantages and disadvantages of the models in order to provide a strong basis for establishing a myocardial fibrosis model.
Highlights
Myocardial fibrosis is a pathological process characterized by cardiomyocyte injury, alterations of the cardiac extracellular matrix, and dysregulated collagen turnover [1]
Hypertensive rat (SHR) is a well model of hereditary hypertension and hypertensive cardiomyopathy [5]. e most commonly used experimental animal is a Wistar inbred rat cultivated by Okamoto in 1963. e spontaneous hypertension in this model is high, which is closely related to the activation of renin-angiotensin-aldosterone system (RASS) [6]
Another research confirmed that a 7-0 prolene suture and an 18-gauge needle were placed around the pulmonary artery, leaving it constricted to the diameter of the needle; four weeks later, rats developed progressive RV hypertrophy accompanied by fibrosis with the mortality rate of 35.71% after surgery [85]
Summary
Myocardial fibrosis is a pathological process characterized by cardiomyocyte injury, alterations of the cardiac extracellular matrix, and dysregulated collagen turnover [1]. As a pathological basis for a variety of heart diseases, it is a potential cause of sudden cardiac death [2]. It usually involves various mechanisms, such as oxidative stress, the renin-angiotensin-aldosterone system (RASS), inflammatory factors, cytokines, vasoactive substances, and signal transduction pathways. Pressure overload, as a common predisposing factor of cardiac remodeling, plays a critical role in the pathogenesis of fibrotic cardiomyopathy [3]. Erefore, selection of a suitable pressure-load-induced myocardial fibrosis model is the primary condition for studying its pathological features, pathogenesis, and treatment. The excellent modeling methods are summarized, with the hope of providing a reference for researchers
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