Macrophage Polarization in Left Ventricular Structural Remodeling Induced by Hypertension

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Following long-term hypertension, mechanical stretching and neuroendocrine stimulation, cause multiple heterogeneous cells of the heart to interact, and result in myocardial remodeling with myocardial hypertrophy and fibrosis. The immune system, specifically macrophages, plays a vital role in this process. Macrophages are heterogeneous and plastic. Regulated by factors such as microenvironment and cytokines, polarization can be divided into two main forms: M1/M2, with different polarizations playing different roles in left ventricular structural remodeling associated with hypertension. However, descriptions of macrophage phenotypes in hypertension-induced myocardial hypertrophy models are not completely consistent. This article summarizes the phenotypes of macrophages in several models, aiming to assist researchers in studying macrophage phenotypes in hypertension-induced left ventricular structural remodeling models.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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