动物造模 z-bio 2021-07-21 630

　　Cardiovascular disease is one of the leading causes of death in the world. According to the World Health Organization, approximately 20 million people died of cardiovascular disease in 2015, and it will continue to be the leading cause of death in the world. Ventricular remodeling is the main reason that various heart diseases eventually develop into heart failure. In diseases such as hypertension, cardiomyopathy, valvular dysfunction, and myocardial infarction, various pathological stimuli such as stress, excessive body fluid, sarcomere gene mutation, neurohumoral activation, etc. can lead to long-term uncontrolled hypertrophy remodeling. As a result, the heart becomes dysfunctional. , And eventually heart failure or cardiac arrest.

　　Recent studies have shown that in the process of myocardial hypertrophy and remodeling caused by different pathogenesis, different inflammatory signal pathways and activation of inflammatory cells will change. The inflammatory signal molecules released by the latter can induce hypertrophy and fibrosis. Recent studies have shown that the inflammatory response initially exists in the heart, is mediated by immune cells mobilized by the heart, precedes the hypertrophy and remodeling of cardiomyocytes, and persists throughout the ventricular remodeling process. ...Early inflammation can help to remove dead cells, promote scar formation and prevent heart rupture. Excessive inflammation can lead to extracellular matrix degradation and apoptosis, ventricular remodeling and heart failure. In the past, people thought that the inflammatory response after heart injury was mainly related to the innate immune response mediated by neutrophils, macrophages and dendritic cells. Recent studies have shown that adaptive immune response plays an important role in ventricular remodeling, and chronic inflammation involving various T cell subgroups is closely related to the development of ventricular remodeling.

　　Naive T lymphocytes are induced to differentiate into different T effector cell subsets and perform different functions in different microenvironments. T cells are mainly divided into helper T cells, regulatory T cells and cytotoxic T cells. Th cells can be subdivided into Th1, Th2, Th17, Th22, Th9 and other subtypes according to the various transcription factors and functions they express. Different T cell subpopulations express different chemokine receptors, mediate the migration and recruitment of different T cell subpopulations, and T cells that move to the inflammatory area perform specific effector functions. Studies have shown that T lymphocytes play an important role in the occurrence and development of ventricular remodeling and heart failure. Recent studies have shown that in a variety of heart diseases, T cells are mobilized into the heart and participate in the pathophysiological process of ventricular remodeling. For many reasons, knocking out mouse T lymphocytes can significantly improve ventricular weight. put up. In a mouse model of cardiac TNF-α overexpression, anti-CD3 antibodies neutralize T cells, reduce the recruitment of inflammatory cells to the heart, and prevent cardiac hypertrophy. In a pressure-overload-induced cardiac hypertrophy model, T cell-deficient ag2 mice have reduced myocardial fibrosis and reduced macrophage infiltration. Another study reported that Rag-1-deficient mice can reduce hypertension and vascular dysfunction caused by vascular tension II, and T cells may be involved in cardiogenic hypertension and remodeling caused by hypertension. Recent studies have shown that in a mouse model of diabetic cardiomyopathy, knocking out CD3 + T cells can improve heart function and reduce myocardial fibrosis.

　　"Further studies have confirmed that T cell subsets such as Th1, Th2, Th17 cells, Tregs and killer T cells play an important role in the repair of myocardial injury and ventricular remodeling.