Aleksandrowicz Marta, Konop Marek, Rybka Mateusz, Mazurek Łukasz, Stradczuk-Mazurek Monika, Kciuk Mateusz, Bądzyńska Bożena, Dobrowolski Leszek, Kuczeriszka Marta
Laboratory of Preclinical Research and Environmental Agents, Mossakowski Medical Research Institute, Polish Academy of Sciences, 5 A. Pawińskiego Street, 02-106 Warsaw, Poland.
Laboratory of Centre for Preclinical Research, Department of Experimental Physiology and Pathophysiology, Medical University of Warsaw, 3C Pawińskiego Street, 02-106 Warsaw, Poland.
Int J Mol Sci. 2025 Jul 4;26(13):6467. doi: 10.3390/ijms26136467.
Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and most of them are connected with atherosclerosis (AS). Hypertension (HT), hyperlipidemia (HPL), and hyperglycaemia (HG) are the main risk factors responsible for CVD and have become a significant public health issue. AS might be a prime causative factor in CVD, and it originates from endothelial cell dysfunction. On the other hand, the factors mentioned above might cause endothelial cell damage as a consequence of endothelial dysfunction (ED) or might be regarded as a consequence of ED. Thus, endothelial cells are critical for maintaining vascular health and homeostasis, and their function is a key contributor to the initiation and progression of AS. The autoregulation of microcirculation, which is functionally present in the brain and kidneys, and from the physiological and pathophysiological point of view, is of high importance to preserve the proper function of the endothelium of blood vessels. The key factor responsible for cardiovascular system regulation and proper action is nitric oxide (). Disturbances in synthesis and/or bioavailability, caused by oxidative stress and/or inflammation, accompany or even precede diseases such as HT, angiogenesis-associated disorders, HPL, and HG, which are on the pathway of AS development. In the present review, we attempted to synthesize recent advances in understanding the pathophysiology of multifactorial-related AS.
心血管疾病（CVDs）是全球主要的死亡原因，其中大多数与动脉粥样硬化（AS）有关。高血压（HT）、高脂血症（HPL）和高血糖（HG）是导致CVD的主要危险因素，并已成为一个重大的公共卫生问题。AS可能是CVD的主要致病因素，它起源于内皮细胞功能障碍。另一方面，上述因素可能由于内皮功能障碍（ED）而导致内皮细胞损伤，或者可能被视为ED的结果。因此，内皮细胞对于维持血管健康和内环境稳定至关重要，其功能是AS发生和发展的关键因素。微循环的自动调节在大脑和肾脏中发挥作用，从生理和病理生理学角度来看，对于维持血管内皮的正常功能非常重要。负责心血管系统调节和正常运作的关键因素是一氧化氮（）。由氧化应激和/或炎症引起的合成和/或生物利用度的紊乱伴随着甚至先于诸如HT、血管生成相关疾病、HPL和HG等疾病，这些疾病都处于AS发展的路径上。在本综述中，我们试图综合近期在理解多因素相关AS病理生理学方面的进展。
