Abstract
The morbidity and mortality of cardiovascular disease (CVD) are relatively high. Studies have shown that most patients with chronic kidney disease (CKD) die from cardiovascular complications. Clinically, the pathophysiological state in which heart disease and kidney disease are causal and influence each other is called cardiorenal syndrome (CRS). Myocardial hypertrophy is the key stage of the heart structure changing from reversible to irreversible. It is an important pathophysiological basis for heart failure. Therefore, this study intends to start with the end-stage uremic phase of CKD to construct an animal model of uremia in rats to study the relationship between uremia, TLR4/MyD88 signaling pathway, and myocardial hypertrophy. The results showed that the uremic rats showed slow weight gain and were thinner. At 12 weeks (w), the serum creatinine and urea nitrogen of the uremic rats increased, and the global hypertrophy index increased. Detecting the expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor (MyD88) in blood samples of rats, we found that the expression of TLR4 and MyD88 increased at 12 w in the uremia group; pathological observation showed that at 4 weeks of uremia model rats, renal tissue compensatory hypertrophy, renal fibrous membrane proliferation, renal parenchyma atrophy, a large number of fibrous proliferation and inflammatory cell infiltration in the interstitium, and protein casts in the renal tubules were observed. Myocardial cells were obviously hypertrophy and disordered. At 12 w, renal tubules were obviously expanded, the epithelium was flat, the brush border disappeared, and the interstitial fibrous connective tissue of the myocardial tissue was proliferated. The detection of TLR4 and MyD88 in kidney tissue and myocardial tissue revealed that the positive expression of TLR4 and MyD88 gradually increased over time. Therefore, the final result of the study is that uremia can gradually lead to myocardial hypertrophy and TLR4 and MyD88 are highly expressed in serum, kidney, and myocardial tissues of uremic rats, suggesting that TLR4 and MyD88 may be related to the degree of uremic disease and the myocardium caused by it. Hypertrophy is related.
Highlights
The morbidity and mortality of cardiovascular disease (CVD) have been high and on the rise, especially in patients with chronic kidney disease (CKD), most of which die from cardiovascular complications. e mortality rate of patients with end-stage CKD complicated by CVD is 10–30 times higher than that of the general population [1]
High blood pressure accelerates the progress of atherosclerosis and promotes heart failure [13]. is study explored the mechanism of myocardial hypertrophy in uremia by establishing uremia model rats
The final result of the study shows that uremia can gradually lead to myocardial hypertrophy and Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) are highly expressed in serum, kidney, and myocardial tissues of uremic rats, suggesting that TLR4 and MyD88 may be related to the degree of uremia and the degree of disease caused by it
Summary
The morbidity and mortality of cardiovascular disease (CVD) have been high and on the rise, especially in patients with chronic kidney disease (CKD), most of which die from cardiovascular complications. e mortality rate of patients with end-stage CKD complicated by CVD is 10–30 times higher than that of the general population [1]. The morbidity and mortality of cardiovascular disease (CVD) have been high and on the rise, especially in patients with chronic kidney disease (CKD), most of which die from cardiovascular complications. E mortality rate of patients with end-stage CKD complicated by CVD is 10–30 times higher than that of the general population [1]. Until now, clinicians have generally recognized that cardiovascular events are the leading cause of death in CKD patients. Upregulation of inflammatory factors and activation of the renin angiotensin aldosterone system (RAAS) in CKD patients in turn increase the production of reactive oxygen species, accelerate the progression of atherosclerosis, and lead to coronary atherosclerotic heart disease. CKD increases the incidence and mortality of cardiovascular events, so the prevention and Evidence-Based Complementary and Alternative Medicine treatment of CVD are important in the management of CKD patients [3]
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