Unveiling Selected Influences on Chronic Kidney Disease Development and Progression

被引:4
作者
Fularski, Piotr [1 ]
Czarnik, Witold [1 ]
Frankenstein, Hanna [1 ]
Gasior, Magdalena [1 ]
Mlynarska, Ewelina [1 ]
Rysz, Jacek [2 ]
Franczyk, Beata [1 ]
机构
[1] Med Univ Lodz, Dept Nephrocardiol, Ul Zeromskiego 113, PL-90549 Lodz, Poland
[2] Univ Lodz, Dept Nephrol Hypertens & Family Med, Ul Zeromskiego 113, PL-90549 Lodz, Poland
关键词
chronic kidney disease; renin-angiotensin-aldosterone system; TGF-beta; 1; vascular calcification; uremic toxins; hypertension; MONOCYTE CHEMOATTRACTANT PROTEIN-1; TRIMETHYLAMINE-N-OXIDE; TISSUE GROWTH-FACTOR; NECROSIS-FACTOR-ALPHA; BOUND UREMIC TOXINS; STAGE RENAL-DISEASE; CYSTATIN-C; ENDOTHELIAL DYSFUNCTION; VASCULAR CALCIFICATION; ANGIOTENSIN-II;
D O I
10.3390/cells13090751
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Currently, more and more people are suffering from chronic kidney disease (CKD). It is estimated that CKD affects over 10% of the population worldwide. This is a significant issue, as the kidneys largely contribute to maintaining homeostasis by, among other things, regulating blood pressure, the pH of blood, and the water-electrolyte balance and by eliminating unnecessary metabolic waste products from blood. What is more, this disease does not show any specific symptoms at the beginning. The development of CKD is predisposed by certain conditions, such as diabetes mellitus or hypertension. However, these disorders are not the only factors promoting the onset and progression of CKD. The primary purpose of this review is to examine renin-angiotensin-aldosterone system (RAAS) activity, transforming growth factor-beta 1 (TGF-beta 1), vascular calcification (VC), uremic toxins, and hypertension in the context of their impact on the occurrence and the course of CKD. We firmly believe that a deeper comprehension of the cellular and molecular mechanisms underlying CKD can lead to an enhanced understanding of the disease. In the future, this may result in the development of medications targeting specific mechanisms involved in the decline of kidney function. Our paper unveils the selected processes responsible for the deterioration of renal filtration abilities.
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页数:18
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