Key result
Both M1 and M2 macrophage phenotypes are present in models of hypertension-induced cardiac structural remodeling, though their specific roles and exact relationship remain unclear.
Why the study?
Descriptions of macrophage phenotypes in hypertension-induced myocardial hypertrophy models are not completely consistent.
This review highlights that both M1 and M2 macrophage phenotypes are actively involved in hypertension-induced left ventricular remodeling, suggesting that future immunotherapies must account for the complex co-expression of these phenotypes.
Answers are grounded in this paper and cite their sources.
Macrophage phenotypes in hypertensive remodeling do not yet guide therapy; leaves open their precise mechanistic roles.
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.
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Wu et al. (2024) conducted a review in Hypertension-induced left ventricular structural remodeling. Macrophage polarization was evaluated. Both M1 and M2 macrophage phenotypes are present in models of hypertension-induced cardiac structural remodeling, though their specific roles and exact relationship remain unclear.
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