Luming Qi

Dyslipidemia is a central driver in the initiation and progression of atherosclerosis (AS). The chronic inflammation and endothelial injury triggered by dyslipidemia are key pathological events in AS development. Elucidating the molecular network underlying dyslipidemia and developing precise interventions are critical for achieving precision prevention and treatment of AS. Recent studies have demonstrated that sterol regulatory element-binding protein 1 (SREBP1) and lipoprotein(a) [Lp(a)] play pivotal roles in the regulation of lipid synthesis and transport. Additionally, gut microbiota-derived metabolites, such as trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), can activate inflammatory pathways and promote lipid deposition via inter-organ signaling axes, thereby accelerating the progression of AS. However, clinical studies have revealed that even when low-density lipoprotein cholesterol (LDL-C) levels are within the recommended range, a significant number of patients continue to experience cardiovascular events. This indicates the widespread presence of "residual risk". Such residual risk is primarily driven by elevated non-high-density lipoprotein cholesterol (non-HDL-C), abnormal levels of Lp(a), and imbalances in the triglyceride to HDL-C (TG/HDL-C) ratio, highlighting the limitations of traditional therapies in comprehensive lipid profile management. Emerging targeted therapies, including proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, small interfering RNA (siRNA)-based treatments, and Lp(a)-lowering agents like pelacarsen, represent promising strategies for more precise lipid modulation. With the continuous advancement of related research, the precise management of AS will increasingly rely on deeper mechanistic insights and individualized therapeutic strategies. Current strategies for AS prevention and treatment focus on understanding key pathways, including lipid metabolism, inflammation, and vascular dysfunction, to develop targeted therapies. The integration of the 2023 Chinese Guidelines for Lipid Management, imaging, and AI-assisted decision-making will promote data-driven, precision medicine. Personalized drug selection, efficacy monitoring, and long-term follow-up will optimize clinical outcomes and enhance prevention strategies for high-risk patients.

Dyslipidemia is a central driver in the initiation and progression of atherosclerosis (AS). The chronic inflammation and endothelial injury triggered by dyslipidemia are key pathological events in AS development. Elucidating the molecular network underlying dyslipidemia and developing precise interventions are critical for achieving precision prevention and treatment of AS. Recent studies have demonstrated that sterol regulatory element-binding protein 1 (SREBP1) and lipoprotein(a) [Lp(a)] play pivotal roles in the regulation of lipid synthesis and transport. Additionally, gut microbiota-derived metabolites, such as trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), can activate inflammatory pathways and promote lipid deposition via inter-organ signaling axes, thereby accelerating the progression of AS. However, clinical studies have revealed that even when low-density lipoprotein cholesterol (LDL-C) levels are within the recommended range, a significant number of patients continue to experience cardiovascular events. This indicates the widespread presence of "residual risk". Such residual risk is primarily driven by elevated non-high-density lipoprotein cholesterol (non-HDL-C), abnormal levels of Lp(a), and imbalances in the triglyceride to HDL-C (TG/HDL-C) ratio, highlighting the limitations of traditional therapies in comprehensive lipid profile management. Emerging targeted therapies, including proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, small interfering RNA (siRNA)-based treatments, and Lp(a)-lowering agents like pelacarsen, represent promising strategies for more precise lipid modulation. With the continuous advancement of related research, the precise management of AS will increasingly rely on deeper mechanistic insights and individualized therapeutic strategies. Current strategies for AS prevention and treatment focus on understanding key pathways, including lipid metabolism, inflammation, and vascular dysfunction, to develop targeted therapies. The integration of the 2023 Chinese Guidelines for Lipid Management, imaging, and AI-assisted decision-making will promote data-driven, precision medicine. Personalized drug selection, efficacy monitoring, and long-term follow-up will optimize clinical outcomes and enhance prevention strategies for high-risk patients.

Background: Sodium intake is undoubtedly essential for normal bodily function, but it is an important public health concern when intake exceeds dietary requirements. With salt intake exceeding recommended levels in almost all countries, high salt intake has become an important global health topic. This study aimed to be the first to combine epidemiological big data with animal behavioral experiments to systematically investigate the association between dietary sodium intake and cognitive function.Methods: Based on NHANES data from 2011 to 2014, the association between dietary sodium intake and cognitive impairment was assessed using multivariate linear regression and five types of machine learning, including random forest and XGBoost, in 2367 participants aged 60–80 years. Cognitive function was further assessed by a 6-month high-salt dietary intervention in a C57BL/6 mouse model combined with behavioral tests such as the Morris water maze and Open Field Test (OFT).Results: The results of the study revealed that the average daily sodium intake of the 2,367 middle-aged and older adults included reached 4,502 mg, with 91% exceeding the recommended standard. Dietary sodium intake was positively correlated with cognitive function scores (p < 0.001). The random forest model had the best predictive efficacy (AUC = 0.918), which was significantly better than that of the SVM and neural networks. Animal behavioral experiments revealed that high-salt dietary exposure significantly impaired neurobehavioral function in a dose-dependent manner, leading to spatial memory deficits and anxious behavior in mice.Conclusion: There was a threshold-dependent association between dietary sodium intake and cognitive function, and the dose–response trend was consistent between human observational studies and animal studies. This study provides translational medical evidence for the public health strategy of “salt reduction for dementia prevention.

High salt intake is a major risk factor for hypertension, and its underlying mechanism may be closely linked to extracellular vesicles (EVs) secreted by gut microbiota. These EVs, produced by gut microbiota, carry various bioactive components that may play a crucial role in the development of hypertension induced by a high-salt diet (HSD). To investigate this mechanism, we developed an efficient extraction method based on density gradient centrifugation to isolate EVs from the gut microbiota of salt-sensitive rats fed an HSD. Through particle size analysis, transmission electron microscopy (TEM), and lipopolysaccharide (LPS) detection, we identified the gradient distribution of gut microbiota EVs and achieved precise extraction. Furthermore, 16S rRNA gene sequencing was employed to analyze the origin and compositional differences of EVs between the normal and HSD groups, revealing the impact of high salt intake on the genetic characteristics of gut microbiota EVs. This study provides valuable tools and scientific insights into the gut microbiota mechanisms underlying salt-induced hypertension and offers new perspectives for the prevention and treatment of related diseases.

High salt intake is a major risk factor for hypertension, and its underlying mechanism may be closely linked to extracellular vesicles (EVs) secreted by gut microbiota. These EVs, produced by gut microbiota, carry various bioactive components that may play a crucial role in the development of hypertension induced by a high-salt diet (HSD). To investigate this mechanism, we developed an efficient extraction method based on density gradient centrifugation to isolate EVs from the gut microbiota of salt-sensitive rats fed an HSD. Through particle size analysis, transmission electron microscopy (TEM), and lipopolysaccharide (LPS) detection, we identified the gradient distribution of gut microbiota EVs and achieved precise extraction. Furthermore, 16S rRNA gene sequencing was employed to analyze the origin and compositional differences of EVs between the normal and HSD groups, revealing the impact of high salt intake on the genetic characteristics of gut microbiota EVs. This study provides valuable tools and scientific insights into the gut microbiota mechanisms underlying salt-induced hypertension and offers new perspectives for the prevention and treatment of related diseases.

Vascular smooth muscle cells (VSMCs) are integral to the pathophysiology of cardiovascular diseases (CVDs). Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase, plays a crucial role in epigenetic regulation of VSMCs gene expression. Emerging researches suggest that EZH2 has a dual role in VSMCs, contingent on the pathological context of specific CVDs. This mini-review synthesizes the current knowledge on the mechanisms by which EZH2 regulates VSMC proliferation, migration and survival in the context of CVDs. The goal is to underscore the potential of EZH2 as a therapeutic target for CVDs treatment. Modulating EZH2 and its associated epigenetic pathways in VSMCs could potentially ameliorate vascular remodeling, a key factor in the progression of many CVDs. Despite the promising outlook, further investigation is warranted to elucidate the epigenetic mechanisms mediated by EZH2 in VSMCs, which may pave the way for novel epigenetic therapies for conditions such as atherosclerosis and hypertension.

The fruit of Phyllanthus emblica L. (FEPE) has a long history of use in Asian folk medicine. The main bioactive compounds in FEPE are polyphenols, known for their potent antioxidant, anti-inflammatory, and hypolipidemic activities. The present study aimed to investigate the intervention effect of FEPE (100 and 200 mg/kg) on hyperlipidemia for 8 weeks and preliminarily explored the potential mechanism by microbiome-metabolome analysis. The results showed that a high-dose FEPE (200 mg/kg) effectively alleviated dyslipidaemic symptoms and body weight gain in hyperlipidemic mice induced by a high-fat diet (HFD). Microbiome analysis showed that FEPE altered the structure of the intestinal microbiota, which included an increase in specific probiotics (such as Akkermansia, Anaerovorax, and Bacteroides) and a decrease in harmful bacteria (including A2, Acetitomaculum, Candidatus_Arthromitus, Lachnospiraceae_NK4A136_group, Lachnospiraceae_NK4B4_group, Rikenella, and Streptococcus), as well as a reduction in the level of short-chain fatty acids (SCFAs). In addition, significant changes in the hepatic metabolome were observed, and eight key metabolites associated with betaine metabolism, lysine degradation, methionine metabolism, and fatty acid metabolism pathways were primarily filtered. The correlated analysis identified several key “microbiota-metabolite” axes in the treatment of hyperlipidemia by FEPE extract. In conclusion, the present study is expected to provide a basis for treating hyperlipidemia with FEPE from the perspective of the microbiome-liver metabolome axis.

Background: The gut microbiota and its stability have important relationships with immunity. However, bibliometric analysis in this field is underdeveloped. This study aims to visualize publications related to the gut microbiota and immunity to identify research frontiers and hotspots, providing references and guidance for further research. Methods: Gut microbiota and immunity data were retrieved from the Web of Science Core Collection database, and Microsoft Excel, Scimago Graphica and VOSviewer software were used to analyze publication output trends, the most productive countries/regions, journals, authors, co-cited references, and keywords. Results: This study analyzed 16,611 publications, including 10,865 articles and 5746 reviews, and found a continuous increase in publications related to gut microbiota and immunity since 2013. We identified 62,872 authors contributing to this field from 2144 journals and 9965 organizations/institutions in 145 countries/regions. The top publisher with the highest output is University of California System with 525 papers. Among these journals, the top 3 most prolific journals are Frontiers in Immunology, Frontiers in Microbiology, and PLOS ONE. The literature with the highest citation frequency is published in Science and has been cited 3006 times by Patrick M. Smith and others. Gut microbiota research hotspots include gut microbiota inflammation, immune response, inflammatory bowel diseases (IBDs), and microbiota tumors. The gut microbiota and its microbial homeostasis play critical roles in immune reactions, inflammation, and even tumors and IBDs. Current research on gut microbiota and immunity is a popular field. Previous studies have shown that the gut microbiota and its microbial species have important effects on maintaining human health, immune function, inflammation, tumorigenesis, and IBDs. Understanding the roles of microbial communities and specific bacterial species as well as their interactions with humans has led to numerous discoveries that provide unique opportunities for exploring human health and future research. Conclusion: This study used bibliometric and visualization analysis to identify the development trends and hotspots of publications related to the gut microbiota and immunity. The findings of this study provide valuable insights into the emerging trends and future directions in this field.