Chongfan Technology
News
21
2024
-
10
Don't drink! Southern Medical University Liu Youhua/Fu Haiyan found that long-term drinking aggravated acute kidney injury
Author:
Alcohol abuse is one of the major public health problems in the world and is associated with various health conditions. However, little is known about the effects of alcohol consumption on acute kidney injury (AKI).
On October 3, 2024, Liu Youhua and Fu Haiyan of Southern Medical University jointly communicatedRedox BiologyPublished online entitled“Chronic alcohol consumption aggaggated acute kidney injury through integrin β1/JNK signaling”The research paper,The studyIt is shown that alcohol consumption increases the susceptibility to AKI in female mice, which may be mediated by the acetaldehyde/integrin β1/JNK signaling cascade.
Studies have demonstrated that chronic and binge drinking of alcohol fed a Lieber-DeCarli diet containing 5% ethanol for 10 days, followed by a single gavage dose of 31.5% ethanol, aggravated AKI after ischemia-reperfusion injury (IRI) in female mice, but not in male mice. EtOH-fed female mice had more severe renal dysfunction, histopathology, and tubular cell apoptosis after IRI than pair-fed controls. RNA sequencing and experimental validation found that activation of integrin β1 and its downstream c-Jun NH2-terminal kinase (JNK) aggravated AKI in EtOH-fed mice. Knockdown of integrin β1 inhibited JNK phosphorylation and reduced AKI in EtOH-fed mice, while agonist antibody activation of integrin β1 increased JNK phosphorylation, aggravated renal tissue injury and tubular cell apoptosis, and aggravated renal dysfunction. In vitro, activation of integrin β1 increases JNK phosphorylation and induces apoptosis in tubular epithelial cells.The deleterious effects of EtOH feeding were primarily mediated by acetaldehyde, as acetaldehyde levels were elevated in the blood, liver and kidney of the ethanol-fed female mice. Acetaldehyde itself activates integrin β1/JNK signaling pathway and induces tubular cell apoptosis in vitro.
Acute kidney injury (AKI) is a clinical syndrome characterized by a sudden decline in renal function.AKI occurs in 10 - 15% of hospitalized patients and more than 50% in intensive care unit (ICU). AKI is associated with a poor prognosis, causing 2 million deaths worldwide each year, and the global burden of associated mortality far exceeds that of breast cancer, heart failure or diabetes. Risk factors for AKI include environmental exposure, toxin intake, surgery, sepsis, unhealthy lifestyle, and genetic background.In this context, understanding the risk factors of AKI and effectively avoiding its occurrence can reduce the occurrence of AKI and improve the treatment effect and prognosis.
Alcohol consumption is one of the major health problems worldwide.According to a recent report by the World Health Organization (WHO), 3 million people die from alcohol abuse every year, accounting for 5.3 percent of the total deaths. In addition, a number of 200 health conditions have been linked to alcohol abuse, including liver disease, cancer, cardiovascular disease and more. Long-term alcohol consumption can cause major changes in several organ systems, including the kidneys. The liver is the main organ that metabolizes alcohol, and about 80% of the intake of ethanol is metabolized in the liver. Three enzyme systems are involved in alcohol metabolism: cytosolic alcohol dehydrogenase (ADH), microsomal ethanol oxidation system (MEOS), and the peroxidase catalase. In most drinkers, chronic heavy drinking can lead to fatty liver disease.1/3 of patients develop alcoholic steatohepatitis (ASH) and 20% eventually develop cirrhosis.
The relationship between alcohol consumption and kidney disease is highly complex and uncertain.AKI is a common complication in patients with cirrhosis and alcoholic hepatitis and is often associated with a poor prognosis. However, the relationship between alcohol consumption and chronic kidney disease (CKD) remains controversial. Some studies suggest that light or moderate alcohol consumption may be associated with a lower risk of CKD, while other studies suggest that alcohol consumption is associated with the onset and accelerated progression of CKD. A large number of experimental studies have shown that alcohol consumption can impair glomerular filtration and tubular reabsorption. In addition, alcohol consumption can impair kidney development, leading to a decrease in the number of nephrons. However, whether there is a strong link between alcohol consumption and AKI remains to be confirmed experimentally.In addition, whether there is a gender difference in susceptibility to AKI after alcohol consumption remains an open question.
The study illustrates that alcohol consumption sensitizes female mice (but not males) to ischemic injury and aggravated AKI, characterized by aggravated renal dysfunction, tubular cell damage, and apoptosis. Through RNA sequencing (RNA-seq) and experimental verification, it was found that integrin β1 and its downstream c-Jun N-terminal kinase (JNK) are the main mediators that play a deleterious role in AKI.The findings provide direct evidence that alcohol consumption is associated with an increased susceptibility to severe AKI following acute injury.
Chongqing Chongfan Technology Co., Ltd. Optical platform film thickness meter OCT optical coherence tomography LabVIEW control
LATEST NEWS
Thank you for visiting the official website of Chongfan Technology. If you have cooperation intentions or suggestions, please contact us through the following methods, and we will reply as soon as possible, thank you!
Address: Room 403, Building 6, Phase III of R&D, No. 36 Xiyong Avenue, High tech Zone, Chongqing, China.
Telephone: +86-13658337211
E-mail: Sales@cfkeji.net
Website: www.cfkeji.net
Mobile Version
