Department of Nephrology, Hypertension and Family Medicine, Medical University of Lodz, ul. Żeromskiego 113, 90-549 Łódź, Poland.
Int J Mol Sci. 2021 Sep 7;22(18):9669. doi: 10.3390/ijms22189669.
Arterial hypertension (AH) is a major risk factor for the development of cardiovascular diseases. It is estimated that the disease affects between 10% and 20% of the adult population and is responsible for 5.8% of all deaths worldwide. Several pathophysiologic factors are crucial in AH, including inappropriate activation of the renin-angiotensin-aldosterone system, oxidative stress and inflammation. The heart, kidney, brain, retina and arterial blood vessels are prime targets of hypertensive damage. Uncontrolled and untreated AH accelerates the damage to these organs and could cause their failure. Damage to these organs could also manifest as coronary heart disease, cognitive impairment, retinopathy or optic neuropathy. For better understanding, it is important to analyze molecular factors which take part in pathogenesis of AH and hypertension-related target organ damage. In our paper, we would like to focus on molecular interactions of AH in the heart, blood vessels, brain and kidneys. We focus on matrix metalloproteinases, the role of immune system, the renin-angiotensin-aldosterone system and oxidative stress in hypertensive induced organ damage.
动脉高血压（AH）是心血管疾病发展的主要危险因素。据估计，该病影响了 10%至 20%的成年人口，占全球所有死亡人数的 5.8%。AH 的几个病理生理因素至关重要，包括肾素-血管紧张素-醛固酮系统的不当激活、氧化应激和炎症。心脏、肾脏、大脑、视网膜和动脉血管是高血压损害的主要靶器官。不受控制和未经治疗的 AH 会加速这些器官的损害，并可能导致它们衰竭。这些器官的损害也可能表现为冠心病、认知障碍、视网膜病变或视神经病变。为了更好地理解，分析参与 AH 发病机制和高血压相关靶器官损害的分子因素非常重要。在本文中，我们将重点研究 AH 在心脏、血管、大脑和肾脏中的分子相互作用。我们关注基质金属蛋白酶、免疫系统的作用、肾素-血管紧张素-醛固酮系统和氧化应激在高血压引起的器官损害中的作用。
