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Atherosclerosis (AS), the main contributor to acute cardiovascular events, such as myocardial infarction and ischemic stroke, is characterized by necrotic core formation and plaque instability induced by cell death. The mechanisms of cell death in AS have recently been identified and elucidated. Ferroptosis, a novel iron-dependent form of cell death, has been proven to participate in atherosclerotic progression by increasing endothelial reactive oxygen species (ROS) levels and lipid peroxidation. Furthermore, accumulated intracellular iron activates various signaling pathways or risk factors for AS, such as abnormal lipid metabolism, oxidative stress, and inflammation, which can eventually lead to the disordered function of macrophages, vascular smooth muscle cells, and vascular endothelial cells. However, the molecular pathways through which ferroptosis affects AS development and progression are not entirely understood. This review systematically summarizes the interactions between AS and ferroptosis and provides a feasible approach for inhibiting AS progression from the perspective of ferroptosis.

In atherosclerosis, macrophage-derived foam cell formation is considered to be a hallmark of the pathological process; this occurs via the uptake of modified lipoproteins. In the present study, we aim to determine the role of transaldolase in foam cell formation and atherogenesis and reveal the mechanisms underlying its role. Bone marrow-derived macrophages (BMDMs) isolated from mice successfully form foam cells after treatment with oxidized low-density lipoprotein (80 μg/mL). Elevated transaldolase levels in the foam cell model are assessed by quantitative polymerase chain reaction and western blot analysis. Transaldolase overexpression and knockdown in BMDMs are achieved via plasmid transfection and small interfering RNA technology, respectively. We find that transaldolase overexpression effectively attenuates, whereas transaldolase knockdown accelerates, macrophage-derived foam cell formation through the inhibition or activation of cholesterol uptake mediated by the scavenger receptor cluster of differentiation 36 (CD36) in a p38 mitogen-activated protein kinase (MAPK) signaling-dependent manner. Transaldolase-mediated glutathione (GSH) homeostasis is identified as the upstream regulator of p38 MAPK-mediated CD36-dependent cholesterol uptake in BMDMs. Transaldolase upregulates GSH production, thereby suppressing p38 activity and reducing the CD36 level, ultimately preventing foam cell formation and atherosclerosis. Thus, our findings indicate that the transaldolase-GSH-p38-CD36 axis may represent a promising therapeutic target for atherosclerosis.

Kidney disease is a serious public health problem and various kidney diseases could progress to end-stage renal disease. The many complications of end-stage renal disease. have a significant impact on the physical and mental health of patients. Ultrasound can be the test of choice for evaluating the kidney and perirenal tissue as it is real-time, available and non-radioactive. To overcome substantial interobserver variability in renal ultrasound interpretation, artificial intelligence (AI) has the potential to be a new method to help radiologists make clinical decisions. This review introduces the applications of AI in renal ultrasound, including automatic segmentation of the kidney, measurement of the renal volume, prediction of the kidney function, diagnosis of the kidney diseases. The advantages and disadvantages of the applications will also be presented clinicians to conduct research. Additionally, the challenges and future perspectives of AI are discussed.

Ferroptosis is a newly identified form of non-apoptotic cell death characterised primarily by iron-dependent lipid peroxidation. It differs morphologically, biochemically, and genetically from other forms of cell death, such as apoptosis, autophagy, and necrosis. Although the molecular mechanism underlying ferroptosis remains unclear, multiple biological processes, such as iron metabolism, lipid peroxides, and systems, such as the glutathione system and the tetrahydrobiopterin/coenzyme Q10 system, appear to be involved. While the contribution of ferroptotic mechanisms to human diseases is not clear, recent studies have identified a number of ferroptosis-related genes. Cardiovascular diseases are the main cause of death globally. In this review, we outline the progress regarding the emerging role of ferroptosis in the pathogenesis of cardiac pathophysiological conditions and the association of ferroptosis with cardiomyopathy, myocardial ischemia-reperfusion injury, heart failure, and atherosclerosis. We further summarise newly discovered ferroptotic targets for the development of therapies for cardiovascular diseases. Finally, we discuss the current challenges and future research directions in cardiovascular disease treatments.

Ultrasound elastography (USE) provides complementary information of tissue stiffness and elasticity to conventional ultrasound imaging. It is noninvasive and free of radiation, and has become a valuable tool to improve diagnostic performance with conventional ultrasound imaging. However, the diagnostic accuracy will be reduced due to high operator-dependence and intra- and inter-observer variability in visual observations of radiologists. Artificial intelligence (AI) has great potential to perform automatic medical image analysis tasks to provide a more objective, accurate and intelligent diagnosis. More recently, the enhanced diagnostic performance of AI applied to USE have been demonstrated for various disease evaluations. This review provides an overview of the basic concepts of USE and AI techniques for clinical radiologists and then introduces the applications of AI in USE imaging that focus on the following anatomical sites: liver, breast, thyroid and other organs for lesion detection and segmentation, machine learning (ML) - assisted classification and prognosis prediction. In addition, the existing challenges and future trends of AI in USE are also discussed.

Purpose. Aloperine (ALO), an alkaloid isolated from Sophora alopecuroides L., possesses multiple pharmacological activities and holds a promise potential for the treatment of various clinical conditions, including skin hypersensitivity, cancer, and inflammatory disorders. The purpose of this study was to investigate the role of ALO in acetaminophen (N‐acetyl‐para‐aminophenol (APAP))‐induced acute liver injury and its underlying mechanisms. Materials and Methods. An animal model of acute liver injury was induced by intraperitoneal injection of APAP (150 mg/kg). Prior to APAP injection, ALO (40 mg/kg) was administered daily for 7 consecutive days. Serum alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase levels were then measured using an automated chemical analyzer. Histopathological changes were evaluated using hematoxylin and eosin staining. Oxidative stress levels were measured by detecting superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA). Pro‐inflammatory cytokines were detected in serum and liver tissues using ELISA and quantitative real‐time polymerase chain reaction (q‐PCR). The expression of members of the HMGB1/TLR4/NF‐κB signaling pathway and NLRP3 inflammasome were determined by Western blot and/or q‐PCR. In addition, the expression and location of NLRP3, cleaved caspase‐1, high‐mobility group box 1 (HMGB1), and phosphorylated p65 (p‐p65) were detected by immunofluorescence. Results. Pretreatment with ALO significantly protected mice from APAP‐induced acute liver injury, with decreased MDA content, and significantly increased GSH and SOD activities. Furthermore, ALO pretreatment reduced the release of pro‐inflammatory cytokines (IL‐1β and TNF‐α) and decreased the expression of caspase‐1, cleaved caspase‐1, and NLRP3. In addition, ALO pretreatment also inhibited the activation of the HMGB1/TLR4/NF‐κB signaling pathway. Conclusion. Taken together, ALO can ameliorate APAP‐induced acute liver injury by inhibiting oxidative stress, inflammation by inhibiting the HMGB1/TLR4/NF‐κB, and NLRP3/inflammasome pathway. [ABSTRACT FROM AUTHOR]

Folate is a water-soluble B vitamin involved in the synthesis of purines and pyrimidines and is one of the essential vitamins for human growth and reproduction. Folate deficiency due to low dietary intake, poor absorption of folate, and alterations in folate metabolism due to genetic defects or drug interactions significantly increases the risk of diseases such as neural tube defects, cardiovascular disease, cancer, and cognitive dysfunction. Recent studies have shown that folate deficiency can cause hyperhomocysteinemia, which increases the risk of hypertension and cardiovascular disease, and that high homocysteine levels are an independent risk factor for liver fibrosis and cirrhosis. In addition, folate deficiency results in increased secretion of pro-inflammatory factors and impaired lipid metabolism in the liver, leading to lipid accumulation in hepatocytes and fibrosis. There is substantial evidence that folate deficiency contributes to the development and progression of a variety of liver diseases, including non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcoholic liver disease (ALD), viral hepatitis, hepatic fibrosis, and liver cancer. Here we review key studies on the role of folate in the pathophysiology of liver diseases, summarize the current status of studies on folate in the treatment of liver diseases, and speculate that folate may be a potential therapeutic target for liver diseases. [ABSTRACT FROM AUTHOR]