Intracranial atherosclerosis （ICAS） is the main cause of ischemic stroke in the world. In clinical practice， ICAS is mainly identified through imaging examinations. In recent years， high-resolution magnetic resonance vessel wall imaging （HRMR-VWI） has gradually become an important means for evaluating the characteristics of ICAS plaques. The application of HRMR-VWI has increased the accuracy in identifying the pathogenesis of acute ischemic stroke， providing a reference for the secondary prevention and clinical individualized treatment of stroke. This article systematically reviews the imaging manifestations of the main components of ICAS plaques on HRMR-VWI， summarizes the progress on HRMR technology， and discusses the relationship between intracranial arterial plaque characteristics and stroke occurrence and recurrence as well as the relationship between plaque characteristics and stroke mechanisms， aiming to provide a basis for the diagnosis and treatment of ICAS-related ischemic stroke.
Atherosclerosis

As a serious cardiovascular disease, atherosclerosis (AS) causes chronic inflammation and oxidative stress in the body and poses a threat to human health. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a member of the phospholipase A2 (PLA2) family, and its elevated levels have been shown to contribute to AS. Lp-PLA2 is closely related to a variety of lipoproteins, and its role in promoting inflammatory responses and oxidative stress in AS is mainly achieved by hydrolyzing oxidized phosphatidylcholine (oxPC) to produce lysophosphatidylcholine (lysoPC). Moreover, macrophage apoptosis within plaque is promoted by localized Lp-PLA2 which also promotes plaque instability. This paper reviews those researches of Chinese medicine in treating AS via reducing Lp-PLA2 levels to guide future experimental studies and clinical applications related to AS.
Humans ; 1-Alkyl-2-acetylglycerophosphocholine Esterase ; Medicine, Chinese Traditional ; Atherosclerosis/drug therapy* ; Lipoproteins ; Plaque, Atherosclerotic ; Biomarkers

Objective To investigate the risk factors for the early progression of atherosclerosis，whether hyperhomocysteinemia （HHcy） is an independent risk factor for the early progression of atherosclerosis， and whether the reduction in homocysteine （Hcy） can delay the early progression of atherosclerosis. Methods The villagers，aged ≥40 years， from Liulin Town of Hanzhong City， Shaanxi Province， China were selected for structured inquiry， carotid ultrasound examination， and blood test in May 2017 and June 2020. Ultrasound examination was performed to measure carotid intima-media thickness （CIMT）， carotid plaque， and carotid stenosis rate to reflect the degree of arteriosclerosis. Results A total of 500 individuals were included in the final analysis， among whom 451 had no CIMT thickening at baseline， 429 had no carotid plaque at baseline， and 454 had no carotid stenosis at baseline. After 3 years of follow-up， among the 500 individuals， 176 （35.2%） had CIMT thickening， and the multivariate analysis showed that old age， smoking， and a high level of low-density lipoprotein cholesterol （LDL-C） were independent risk factors for CIMT thickening； 252 （50.4%） had new-onset plaques， and the multivariate analysis showed that old age， hypertension， and high LDL-C were independent risk factors for plaque formation； 231（46.2%） had new-onset carotid stenosis， and the multivariate analysis showed that old age， high LDL-C， and elevated triglyceride were independent risk factors for carotid stenosis. There were 364 patients with HHcy （≥15 μmol/L） in the initial examination， and after 3 years， 119 had a reduction in Hcy， while 245 had no reduction in Hcy. After adjustment for sex， previous stroke， smoking， baseline LDL-C， baseline Hcy， and Hcy after 3 years， the multivariate analysis showed that neither HHcy nor the reduction in Hcy was associated with carotid atherosclerosis. Conclusion Old age， high LDL-C， smoking， and hypertension are the main risk factors for atherosclerosis in villagers aged ≥40 years in rural areas of Hanzhong City in Shaanxi Province. There is no significant association between HHcy and carotid atherosclerosis， and the reduction in Hcy cannot delay or reverse the process of carotid atherosclerosis.
Atherosclerosis ; Homocysteine

Atherosclerosis is the main etiology of tandem occlusion in patients with acute ischemic stroke， with the possible mechanisms of in situ thrombosis due to atherosclerosis or distal arterial embolization due to the dislodgment of partial thrombi or plaques. The atherosclerotic elements identified within the thrombus or emboli can help with the diagnosis of the etiology of occlusion and the evaluation of plaques. This article reports a case of acute ischemic stroke due to tandem occlusion of the right anterior circulation， and the dislodgment of thrombi occurred during internal carotid artery angioplasty. The pathological analysis of the thrombi revealed a large amount of cholesterol crystals， which helped with the etiological classification of stroke and the evaluation of plaques.
Atherosclerosis

BACKGROUND: Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) are the main causes of restenosis (RS) in diabetic lower extremity arterial disease (LEAD). However, the relevant pathogenic mechanisms are poorly understood. METHODS: In this study, we introduced a "two-step injury protocol" rat RS model, which started with the induction of atherosclerosis (AS) and was followed by percutaneous transluminal angioplasty (PTA). Hematoxylin-eosin (HE) staining and immunohistochemistry staining were used to verify the form of RS. Two-step transfection was performed, with the first transfection of Lin28a followed by a second transfection of let-7c and let-7g, to explore the possible mechanism by which Lin28a exerted effects. 5-ethynyl-2΄-deoxyuridine (EdU) and Transwell assay were performed to evaluate the ability of proliferation and migration of VSMCs. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were performed to detect the expression of Lin28a protein and let-7 family members. RESULTS: Using a combination of in vitro and in vivo experiments, we discovered that let-7c, let-7g, and microRNA98 (miR98) were downstream targets of Lin28a. More importantly, decreased expression of let-7c/let-7g increased Lin28a, leading to further inhibition of let-7c/let-7g. We also found an increased level of let-7d in the RS pathological condition, suggesting that it may function as a protective regulator of the Lin28a/let-7 loop by inhibiting the proliferation and migration of VSMCs. CONCLUSION These findings indicated the presence of a double-negative feedback loop consisting of Lin28a and let-7c/let-7g, which may be responsible for the vicious behavior of VSMCs in RS.
Rats ; Animals ; Down-Regulation ; MicroRNAs/metabolism* ; Feedback ; Cell Proliferation/genetics* ; Atherosclerosis

BACKGROUND: Atherosclerosis-related diseases represent significant health issues among adults globally. Despite their widespread impact, comprehensive data concerning the global and national burden and trends of these diseases remain sparse. Our objective is to examine the trends in the burden of atherosclerosis among adults from 1990 to 2019 at both global and national levels. METHODS: We reported the average annual percentage changes (AAPCs) in prevalence, incidence, mortality, and disability-adjusted life years (DALYs) of atherosclerosis-related diseases (ischemic heart disease [IHD], ischemic stroke, and peripheral arterial disease [PAD]) at the global and national levels among individuals based on a trend analysis of the Global Burden of Diseases Study (GBD) 2019. We further analyzed these global trends as a function of age, gender, and the social development index. We also used joinpoint regression analysis to identify the year with the most substantial changes in global trends. RESULTS: Globally, the AAPC of IHD incidence rose from 1990 to 2019 (0.20; 95% confidence interval [CI], 0.12-0.28), with substantial surges in 1995, 2001, 2005, 2010, and 2017. Conversely, AAPC of IHD mortality rates exhibited a different trend until a rise in 2014. The AAPC of incidence rates of ischemic stroke and PAD also escalated during the same period, with respective 0.43 (95% CI, 0.39-0.48) and 0.13 (95% CI, 0.06-0.21). For ischemic stroke, both incidence and mortality soared in 2014, while PAD incidence declined in 1994 and 1998, then sharply climbed in 2016. Nationally, the Northern Mariana Islands experienced the steepest increase in IHD and PAD incidence and mortality between 1990 and 2019. China saw a significant rise in ischemic stroke incidence, whereas the highest mortality rate increase occurred in Timor-Leste. By sociodemographic index (SDI) quintile, low-middle-, middle-, and high-middle-SDI countries all showed upward trends in IHD, ischemic stroke, and PAD incidence. Simultaneously, IHD and ischemic stroke mortality rates, as well as DALYs, dropped in the low-, high-middle-, and high-SDI nations. However, PAD mortality rates and DALYs saw an uptick across all SDI quintiles. Regarding age demographics, a global decrease in the AAPC IHD incidence as noted in individuals above 55 years old, in contrast to an increase in the 20-55 age group during this period. AAPC of mortality rates for IHD, ischemic stroke, and PAD decreased across all ages. The AAPC showed an increase in IHD incidence in both genders. Conversely, IHD's DALYs saw a reduction in both males and females. Ischemic stroke patterns mirrored these trends, whereas all measures for PAD exhibited growth for both sexes. CONCLUSIONS From 1990 to 2019, there was an overall increasing trend in the global incidence of all three clinical manifestations of atherosclerosis. Between 1990 and 2019, both the mortality rate and DALYs for IHD and ischemic stroke declined across all age groups. Overall, the burden of atherosclerosis-related diseases has not significantly decreased and even shows signs of trending upward. These findings strongly suggest that despite some progress made, efforts to control atherosclerosis diseases globally need to be intensified.
Adult ; Humans ; Male ; Female ; Middle Aged ; Global Burden of Disease ; Quality-Adjusted Life Years ; Atherosclerosis/epidemiology* ; Myocardial Ischemia/epidemiology* ; Incidence ; Ischemic Stroke

Inflammation is a major underlying mechanism in the progression of numerous cardiovascular diseases (CVDs). Regulatory T cells (Tregs) are typical immune regulatory cells with recognized immunosuppressive properties. Despite the immunosuppressive properties, researchers have acknowledged the significance of Tregs in maintaining tissue homeostasis and facilitating repair/regeneration. Previous studies unveiled the heterogeneity of Tregs in the heart and aorta, which expanded in CVDs with unique transcriptional phenotypes and reparative/regenerative function. This review briefly summarizes the functional principles of Tregs, also including the synergistic effect of Tregs and other immune cells in CVDs. We discriminate the roles and therapeutic potential of Tregs in CVDs such as atherosclerosis, hypertension, abdominal arterial aneurysm, pulmonary arterial hypertension, Kawasaki disease, myocarditis, myocardial infarction, and heart failure. Tregs not only exert anti-inflammatory effects but also actively promote myocardial regeneration and vascular repair, maintaining the stability of the local microenvironment. Given that the specific mechanism of Tregs functioning in CVDs remains unclear, we reviewed previous clinical and basic studies and the latest findings on the function and mechanism of Tregs in CVDs.
Humans ; T-Lymphocytes, Regulatory ; Cardiovascular Diseases ; Atherosclerosis ; Myocardial Infarction ; Phenotype

Lipids droplets are organelles that store neutral lipids and are closely related to lipid accumulation. Long chain acyl-coenzyme A synthetase 3 (ACSL3) is a lipid droplet-associated protein mainly distributed in the cell membrane, endoplasmic reticulum, and intracellular lipid droplets, and its distribution depends on cell type and fatty acid supply. ACSL3 is a key regulator of fatty acid metabolism that is closely related to intracellular lipid accumulation, and plays an important role in various pathophysiological processes such as lipid droplet synthesis and lipid metabolism, cellular inflammation, and ferroptosis. This paper mainly reviews the role of ACSL3 in lipid synthesis, ferroptosis, and inflammatory response, with focus on the mechanism of its role in lipid accumulation in atherosclerosis, and provides new ideas for exploring potential therapeutic targets in atherosclerotic diseases.
Humans ; Atherosclerosis ; Coenzyme A Ligases/metabolism* ; Endoplasmic Reticulum/metabolism* ; Fatty Acids/metabolism* ; Lipid Metabolism

Hyperhomocysteinemia (HHcy) is considered to be an independent risk factor for cardiovascular diseases, but the molecular mechanisms underlying its pathogenesis are not fully understood. Endothelial dysfunction is a key initiating factor in the pathogenesis of atherosclerosis, which is commonly observed in almost all HHcy-induced vascular diseases. HHcy promotes oxidative stress, inhibits nitric oxide production, suppresses hydrogen sulfide signaling pathway, promotes endothelial mesenchymal transition, activates coagulation pathways, and promotes protein N-homocysteination and cellular hypomethylation, all of which can cause endothelial dysfunction. This article reviews the specific links between HHcy and endothelial dysfunction, and highlights recent evidence that endothelial mesenchymal transition contributes to HHcy-induced vascular damage, with a hope to provide new ideas for the clinical treatment of HHcy-related vascular diseases.
Humans ; Atherosclerosis ; Cardiovascular Diseases ; Endothelium, Vascular ; Homocysteine/metabolism* ; Hyperhomocysteinemia/complications* ; Oxidative Stress ; Risk Factors

OBJECTIVE: This study aimed to investigate the association between fruit and vegetable intake and arterial stiffness. METHODS: We conducted a cohort-based study comprising 6,628 participants with arterial stiffness information in the Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) project. A semi-quantitative food-frequency questionnaire was used to assess baseline (2007-2008) and recent (2018-2021) fruit and vegetable intake. We assessed changes in fruit and vegetable intake from 2007-2008 to 2018-2021 in 6,481 participants. Arterial stiffness was measured using the arterial velocity-pulse index (AVI) and arterial pressure-volume index (API). Elevated AVI and API values were defined according to diverse age reference ranges. RESULTS: Multivariable-adjusted linear regression models revealed that every 100 g/d increment in fruit and vegetable intake was associated with a 0.11 decrease in AVI ( B= -0.11; 95% confidence interval [ CI]: -0.20, -0.02) on average, rather than API ( B = 0.02; 95% CI: -0.09, 0.13). The risk of elevated AVI (odds ratio [ OR] = 0.82; 95% CI: 0.70, 0.97) is 18% lower in individuals with high intake (≥ 500 g/d) than in those with low intake (< 500 g/d). Furthermore, maintaining a high intake in the past median of 11.5 years of follow-up was associated with an even lower risk of elevated AVI compared with a low intake at both baseline and follow-up ( OR = 0.64; 95% CI: 0.49, 0.83). CONCLUSION Fruit and vegetable intake was negatively associated with arterial stiffness, emphasizing recommendations for adherence to fruit and vegetable intake for the prevention of arterial stiffness.
Humans ; Vascular Stiffness ; Fruit ; Vegetables ; Atherosclerosis ; China