Molecular Mechanisms Underlying Vascular Remodeling in Hypertension

Xinyi Zeng, Yan Yang
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Abstract

Hypertension, a common cardiovascular disease, is primarily characterized by vascular remodeling. Recent extensive research has led to significant progress in understanding its mechanisms. Traditionally, vascular remodeling has been described as a unidirectional process in which blood vessels undergo adaptive remodeling or maladaptive remodeling. Adaptive remodeling involves an increase in vessel diameter in response to increased blood flow, while maladaptive remodeling refers to the narrowing or thickening of blood vessels in response to pathological conditions. However, recent research has revealed that vascular remodeling is much more complex. It is now understood that vascular remodeling is a dynamic interplay between various cellular and molecular events. This interplay process involves different cell types, including endothelial cells, smooth muscle cells, and immune cells, as well as their interactions with the extracellular matrix. Through these interactions, blood vessels undergo intricate and dynamic changes in structure and function in response to various stimuli. Moreover, vascular remodeling involves various factors and mechanisms such as the renin-angiotensin-aldosterone system (RAS), oxidative stress, inflammation, the extracellular matrix (ECM), sympathetic nervous system (SNS) and mechanical stress that impact the arterial wall. These factors may lead to vascular and circulatory system diseases and are primary causes of long-term increases in systemic vascular resistance in hypertensive patients. Additionally, the presence of stem cells in adventitia, media, and intima of blood vessels plays a crucial role in vascular remodeling and disease development. In the future, research will focus on examining the underlying mechanisms contributing to hypertensive vascular remodeling to develop potential solutions for hypertension treatment. This review provides us with a fresh perspective on hypertension and vascular remodeling, undoubtedly sparking further research efforts aimed at uncovering more potent treatments and enhanced preventive and control measures for this disease
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高血压血管重塑的分子机制
高血压是一种常见的心血管疾病,其主要特征是血管重塑。最近的广泛研究使人们在了解其机制方面取得了重大进展。传统上,血管重塑被描述为一个单向过程,即血管发生适应性重塑或不适应性重塑。适应性重塑是指血管直径随着血流量的增加而增大,而适应性重塑是指血管在病理情况下变窄或变厚。然而,最近的研究发现,血管重塑要复杂得多。现在人们已经明白,血管重塑是各种细胞和分子事件之间的动态相互作用。这一相互作用过程涉及不同类型的细胞,包括内皮细胞、平滑肌细胞和免疫细胞,以及它们与细胞外基质的相互作用。通过这些相互作用,血管的结构和功能会在各种刺激下发生复杂而动态的变化。此外,血管重塑涉及各种因素和机制,如影响动脉壁的肾素-血管紧张素-醛固酮系统(RAS)、氧化应激、炎症、细胞外基质(ECM)、交感神经系统(SNS)和机械应力。这些因素可能导致血管和循环系统疾病,也是高血压患者全身血管阻力长期增加的主要原因。此外,干细胞存在于血管的前膜、中膜和内膜,在血管重塑和疾病发展中起着至关重要的作用。未来的研究将重点关注导致高血压血管重塑的潜在机制,以开发治疗高血压的潜在解决方案。这篇综述为我们提供了一个关于高血压和血管重塑的全新视角,无疑将引发进一步的研究工作,旨在发现更有效的治疗方法,并加强该疾病的预防和控制措施。
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