期刊
CELLS
卷 12, 期 13, 页码 -出版社
MDPI
DOI: 10.3390/cells12131679
关键词
atherosclerosis; senescence; chronic kidney disease; inflammation; statins
类别
Chronic kidney disease (CKD) is a severe health problem that affects multiple systems in the human body. Kidney dysfunction is closely related to cardiovascular disease (CVD) due to mechanisms of cellular aging and inflammation. As kidney function deteriorates, the risk of cardiovascular events and mortality increases in CKD patients. Oxidative stress and inflammation are interrelated processes that initiate a vicious cycle. Aging, oxidative stress, and inflammation are major contributors to the development and progression of CVD in CKD patients.
Chronic kidney disease (CKD) is a serious health problem that can affect various systems in the human body. Renal failure promotes mechanisms of premature cellular aging and also features of generalized inflammation in the body, which translates into a close relationship between kidney dysfunction and cardiovascular disease (CVD). As kidney function deteriorates, cardiovascular risk and mortality increase in this group of patients. Oxidative stress and inflammation are two closely related processes that initiate a vicious cycle by activating each other. Together with aging, they represent the key factors that cause and exacerbate CVD in CKD. Patients with CKD are particularly vulnerable to the accumulation of aging endothelial cells, vascular smooth muscle and macrophages, increasing the risk of atherosclerosis. Several mechanisms are known that can lead to the progression of the aforementioned problems, such as the accumulation of uremic toxins, persistent inflammation, impaired lipid and electrolyte metabolism, nitric oxide (NO) deficiency, the increased production of reactive oxygen species (ROS) and damage to deoxyribonucleic acid (DNA) and mitochondria. According to research, we can distinguish a group of drugs that effectively counteract the negative effects of CKD-statins. This is a group of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme-A (HMG-CoA) reductase and affect a number of cellular processes and pathways, resulting in the overall slowing of atherosclerosis and cellular aging.
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