scholarly journals Renal Injury by SARS-CoV-2 Infection: A Systematic Review

2020 ◽  
pp. 1-11
Author(s):  
Mo Wang ◽  
Huaying Xiong ◽  
Han Chen ◽  
Qiu Li ◽  
Xiong Zhong Ruan

<b><i>Background:</i></b> SARS-CoV-2 infection can cause renal involvement, and severe renal dysfunction is more common among patients with chronic comorbid conditions, especially patients with chronic kidney disease. Angiotensin-converting enzyme 2 (ACE2) has been proven to be the major receptor of SARS-CoV-2 in kidneys, suggesting that ACE2-related changes may be involved in renal injury during the infection. In this review, we systematically reviewed the literature to summarize findings on the mechanism of renal injury caused by SARS-COV-2 infection, in order to provide a theoretical basis for renal protection therapy. <b><i>Summary:</i></b> For patients with SARS-CoV-2 infection, renal injury mainly manifests as increased serum creatinine, variable degrees of proteinuria and hematuria, and radiographic abnormalities of the kidneys. In this review, we summarize the pathogenesis of renal injury deriving from SARS-CoV-2 infection by focusing on its etiology, pathology, and clinical manifestations. The virus causes kidney injury by either direct infection or systemic effects, including host immune clearance and immune tolerance disorders, endothelium-mediated vasculitis, thrombus formation, glucose and lipid metabolism disorder, and hypoxia. <b><i>Key Messages:</i></b> Renal injury by SARS-CoV-2 is the result of multiple factors. Via highly expressed ACE2 in renal tissue, SARS-CoV-2 infection fundamentally initiates a mechanism of renal injury. Systemic effects such as host immune clearance and immune tolerance disorders, endothelial cell injury, thrombus formation, glucose and lipid metabolism disorder, and hypoxia aggravate this renal injury.

2019 ◽  
Vol 51 (9) ◽  
pp. 890-899
Author(s):  
Xiaoyu Wang ◽  
Jiajie Zhou ◽  
Manlu Shen ◽  
Jiayan Shen ◽  
Xinyue Zhang ◽  
...  

Abstract Chlorpyrifos (CPF) is a widely used insecticide in pest control, and it can affect aquatic animals by contaminating the water. In this study, larval zebrafish were exposed to CPF at concentrations of 30, 100 and 300 μg/l for 7 days. In the CPF-treated group, lipid droplet accumulation was reduced in larval zebrafish. The levels of triglyceride (TG), total cholesterol (TC), and pyruvate were also decreased after CPF exposure. Cellular apoptosis were significantly increased in the heart tissue after CPF exposure compared with the control. Transcription changes in cardiovascular genes were also observed. Through transcriptome analysis, we found that the transcription of 465 genes changed significantly, with 398 upregulated and 67 downregulated in the CPF-treated group, indicating that CPF exposure altered the transcription of genes. Among these altered genes, a number of genes were closely related to the glucose and lipid metabolism pathways. Furthermore, we also confirmed that the transcription of genes related to fatty acid synthesis, TC synthesis, and lipogenesis were significantly decreased in larval zebrafish after exposure to CPF. These results indicated that CPF exposure induced lipid metabolism disorders associated with cardiovascular toxicity in larval zebrafish.


2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jing Peng ◽  
Qingde Li ◽  
Keye Li ◽  
Li Zhu ◽  
Xiaoding Lin ◽  
...  

Glucose and lipid metabolism disorder in diabetes mellitus often causes damage to multiple tissues and organs. Diabetes mellitus is beneficially affected by quercetin. However, its concrete mechanisms are yet to be fully elucidated. In our study, diabetes was induced in Sprague-Dawley rats by STZ injection. The rats were randomly divided into normal control, diabetic model, low-dose quercetin treatment, high-dose quercetin treatment, and pioglitazone treatment groups. Fasting blood glucose was collected to evaluate diabetes. Immunohistochemistry and fluorometric assay were performed to explore SIRT1. Akt levels were measured through immunoprecipitation and Western blot. After 12 weeks of quercetin treatment, the biochemical parameters of glucose and lipid metabolism improved to varying degrees. Hepatic histomorphological injury was alleviated, and hepatic glycogen content was increased. The expression and activity of hepatic SIRT1 were enhanced, and Akt was activated by phosphorylation and deacetylation. These results suggested that the beneficial effects of quercetin on glucose and lipid metabolism disorder are probably associated with the upregulated activity and protein level of SIRT1 and its influence on Akt signaling pathway. Hence, quercetin shows potential for the treatment of glucose and lipid metabolism disorder in diabetes mellitus.


2015 ◽  
Vol 6 (3) ◽  
pp. 902-909 ◽  
Author(s):  
Kaiping Wang ◽  
Peng Cao ◽  
Weizhi Shui ◽  
Qiuxiang Yang ◽  
Zhuohong Tang ◽  
...  

Hypoglycemic and hypolipidemic effects of ASP in prediabetic and T2DM mice.


2021 ◽  
Vol 17 (2) ◽  
pp. 402-416
Author(s):  
Hengzhi Du ◽  
Yanru Zhao ◽  
Zhongwei Yin ◽  
Dao Wen Wang ◽  
Chen Chen

2021 ◽  
Vol 28 ◽  
Author(s):  
Adel Hajj Ali ◽  
Nour Younis ◽  
Rola Abdallah ◽  
Farah Shaer ◽  
Ali Dakroub ◽  
...  

: Cardiovascular disease (CVD) remains the primary cause of global morbidity and mortality. CVD includes various life-threatening conditions such as myocardial infarction, stroke and peripheral arterial diseases. In this context, atherosclerosis continues to play the principal role in the pathogenesis of these conditions. Atherosclerosis emanates from a set of modifiable and non-modifiable risk factors that include age, male gender, family history, obesity, smoking, diabetes mellitus and hypertension. Recent evidence classifies atherosclerosis as a latent disease affecting all-sized arteries with a predilection for arterial branching points of decreased or absent blood supply. Atherosclerosis is not only a lipid metabolism disorder, but is also a chronic inflammatory one. In this review, we provide a synoptic discussion of the underlying pathological mechanisms of atherosclerosis along with the currently applied therapeutic interventions. We then discuss the classical lipid-lowering therapies as well as the newly discovered therapies. For the classical therapies, we point out the importance of statins and ezetimibe in reducing plasma cholesterol levels by virtue of their effects on synthesis, reuptake and intestinal absorption of cholesterol. We also discuss the role of fibrates in modulating lipid metabolism and improving the ratio of high-density to low-density density lipoproteins. We then focus on the more recent molecular and genetic interventions exemplified by proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies, evinacumab, and microRNA inhibitors. Special attention is also given to clinical trials involving these therapies.


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