Morphological and Functional Characteristics of Animal Models of Myocardial Fibrosis Induced by Pressure Overload

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.

Polyphenolic compounds of amla prevent oxidative stress and fibrosis in the kidney and heart of 2K1C rats

“…These preventive effects could be attributed to amla powder's high capacity of scavenging free radicals in tissues. The 2K1C surgery‐induced kidney injury leads to the subsequent development of oxidative stress and fibrosis and for decades, 2K1C model has been used as a suitable animal model for kidney disease research (Ding et al., 2020). It has been postulated that oxidative stress plays a major role in the molecular mechanism involved in the experimental kidney damage of such animal models.…”

“…In the two‐kidneys‐one‐clip model (2K1C), a clip is placed on the renal artery of the left kidney (Mullins et al, 2016). The 2K1C model is similar to the volume overload form of hypertension, and rats are generally used in this animal model for well understanding of angiotensin II‐mediated hypertension and related complications in kidney and hearts (Ding et al., 2020).…”

Changes of myocardial fibrosis markers with the use of beta-blockers and mineralocorticoid receptor antagonists in patients with heart failure with mid-range ejection fraction of ischemic origin

“…Соединительная ткань миокарда играет важную роль в определении и сохранении нормальной архитектуры и функции миокарда. Избыточное отложение коллагена во внеклеточном матриксе приводит к повышенной жесткости миокарда и впоследствии к диастолической дисфункции ЛЖ [14], повышенный синтез/деградация коллагена был обнаружен при сердечной недостаточности, но роль фиброза в диастолической и систолической сердечной недостаточности у больных с промежуточной ФВ требует дальнейшего изучения.…”

Effect of therapy on the dynamics of collagen metabolism markers in older patients with heart failure with mid-range ejection fraction and coronary artery disease

“…Избыточное отложение коллагена во внеклеточном матриксе может привести к повышенной жесткости миокарда и впоследствии к гипертрофии сердца и дисфункции левого желудочка [4]. Одними из наиболее изученных маркеров коллагенобразования на данный момент являются: семейство матриксных металлопротеиназ (MMП) и их тканевые ингибиторы, маркеры угнетения деградации коллагена (ТИМП).…”