The components of coffee exert multifaceted effects on skin health. Studies have shown that caffeine promotes autophagy and scavenges reactive oxygen species, significantly reducing oxidative stress, thereby delaying skin aging and enhancing skin elasticity. Chlorogenic acid, through its antioxidant and anti-inflammatory properties, inhibits the production of inflammatory factors and mitigates skin inflammation, consequently slowing skin aging and reducing the risk of skin cancer. Ferulic acid, derived from the partial degradation of chlorogenic acid during coffee bean roasting, not only exhibits anti-inflammatory and antioxidant functions but also absorbs and reflects ultraviolet (UV) radiation, helping to reduce UV-induced DNA damage and enhance the skin barrier function. Furthermore, caffeine stimulates the proliferation and migration of skin cells, thereby accelerating wound healing. This article elaborates on the roles and potential mechanisms of coffee consumption in delaying skin aging, preventing skin cancer, providing photoprotection, and promoting skin repair and regeneration, highlighting the significance and potential applications of coffee and its bioactive constituents in promoting skin health.

Depression is a prevalent mental disorder characterized by a multifaceted pathogenesis involving theories such as neurotransmitter dysregulation, microglial activation, hypothalamicpituitary-adrenal (HPA) axis dysregulation, inflammasome activation, microbiome alterations, and impaired neuroplasticity. Current first-line antidepressants, including selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), exhibit limitations such as delayed onset, low efficacy rates, and significant interindividual variability. In recent years, driven by advances in molecular biology and immunopsychiatry research, growing evidence has indicated an interplay between immune-inflammatory pathways and depression. The kynurenine pathway, a predominant route for tryptophan metabolism, generates metabolites that play significant roles in neural, immune, and inflammatory regulation, particularly exhibiting complex dual effects in immune modulation. It is essential to construct a comprehensive view of the peripheral-central immune network and delve into the mechanistic role of the tryptophankynurenine metabolic pathway within this network in the pathogenesis of depression, thus further advancing our knowledge of the pathophysiological mechanisms of depression and facilitating drug development.

2025年10月6日,诺贝尔生理学或医学奖授予两位美国科学家Mary E. Brunkow 和Frederick J. Ramsdell,以及日本科学家Shimon Sakaguchi, 以表彰他们在阐明外周免疫耐受关键机制方面所作的开创性贡献:他们成功鉴定出调节性T 细胞, 并揭示了免疫系统如何通过该类细胞维持自身稳态, 防止过度的免疫应答及自身免疫性疾病发生, 这也是一项“迟到了 30 年”的诺奖发现(https://www.nobelprize. org/prizes/medicine/ 2025/summary/) 全文请点击PDF链接至知网下载浏览。 。

Acne vulgaris is a common chronic inflammatory skin disease that affects a wide range of adolescents and some adults. As a globally consumed beverage, coffee's effects on skin health, particularly on acne vulgaris, have attracted increasing attention. Research suggests that coffee constituents, such as caffeine and chlorogenic acid, may exert beneficial effects on acne suppression through their antioxidant, anti-inflammatory, and lipid-regulatory properties. Additionally, coffee may indirectly influence skin health by modulating the gut microbiota through the gut-skin axis. However, the effects of coffee consumption are significantly influenced by individual variability, and additives such as sugar and dairy products in coffee may exacerbate inflammation, potentially counteracting its benefits. This review summarizes current evidence regarding the effects and potential mechanisms of coffee and its major components on acne vulgaris, aiming to provide a theoretical basis and scientific guidance for understanding the potential link between coffee consumption and skin health.

Single-cell RNA sequencing (scRNA-seq) is a high-throughput sequencing technology that profiles genome-wide gene expression at the single-cell level,and can efficiently resolve cellular heterogeneity.It is widely applied in fields such as developmental biology and disease research. However,scRNA-seq data often exhibit characteristics such as high noise,high dimensionality, and high sparsity,which pose significant challenges to traditional data analysis methods.In recent years,deep learning models,represented by autoencoders and generative adversarial networks, have been extensively applied to scRNA-seq data analysis tasks,including expression imputation, batch effect correction,dimensionality reduction,cell clustering,and cell type annotation. These applications demonstrate the power of deep learning. Notably, Transformer-based deep learning models, leveraging self-attention mechanisms to capture implicit dependencies among genes and associations between gene expression and cells, offer a novel strategy and direction for scRNA-seq data analysis, and provide innovative solutions with promising applications for the integration of multimodal omics data.

Proteins serve as the fundamental building blocks of life processes. Their functions are highly determined by the spatial structure, making analyzing these spatial structures essential for fully comprehending their roles. The application of artificial intelligence (AI) models has significantly advanced the development of algorithms for predicting protein spatial structure. AlphaFold2 represents a groundbreaking advancement in this field, enabling rapid, accurate, and large-scale predictions of protein spatial structures. In the AlphaFold era, substantial progress has been made in fields such as protein language model development, protein-protein interaction prediction, and protein design, with notable models including ESM2, ScanNet, RFdiffusion, and RoseTTAFold-All Atom, among others. These novel AI-based algorithms have profoundly facilitated research into protein function, disease mechanisms, and drug design.

Metabolic dysfunction-associated fatty liver disease (MAFLD) is the most prevalent chronic liver disease worldwide, garnering significant attention due to its close association with metabolic disorders. The pathogenesis of MAFLD involves lipid metabolism dysfunction, lipid oxidation, and gene dysregulation. This article focuses on analyzing metabolic pathways in the liver, including hepatic fatty acid uptake, de novo triglyceride synthesis, and lipid oxidation, as well as the functions of associated lipid metabolism genes, such as FATP2, FATP5, CD36, PPARα, CPT1, CPT2, FGF21, SREBP1, ChREBP, ACLY, ACC, FASN, SCD, DGAT2, GPR75, RBP4, adiponectin, and osteocalcin. Through in-depth analysis of these genes and signaling pathways, this article provides new insights and a theoretical basis for the diagnosis and treatment of MAFLD, highlighting the pivotal role of lipid metabolism regulation in the progression of MAFLD, and identifying relevant genes and molecules as potential therapeutic targets.

As one of the most widely consumed beverages globally, coffee's relationship with digestive health has drawn significant attention. Recent studies indicate that coffee exerts bidirectional regulatory effects on the occurrence and progression of gastric ulcers. On one hand, polyphenolic compounds such as chlorogenic acid in coffee exert protective effects on the gastric mucosa by inhibiting inflammatory responses and promoting the growth of beneficial gastrointestinal bacteria. On the other hand, caffeine stimulates gastric acid secretion through multiple signaling pathways, potentially increasing the risk of ulcer development. This article systematically elucidates the regulatory mechanisms of coffee's bioactive constituents in the pathological progression of gastric ulcers, based on evidence from in vivo, in vitro, and clinical studies. It further analyzes the association between coffee consumption and gastric ulcer risk across different populations. The aim is to provide scientific recommendations for coffee consumption to the public and to offer a theoretical basis for further research and applications of coffee in digestive health.

The rapid accumulation of biological big data, primarily comprising genomics, transcriptomics, proteomics, and more, coupled with the swift advancement of artificial intelligence technologies, notably deep learning, has given rise to a variety of biological large models. Characterized by complex deep-learning architectures, massive parameter counts, high computational power requirements, and vast amounts of pre-training data, these large models' capabilities are largely dictated by the types and volumes of pre-training data, while different model architectures support various downstream tasks. Over the past two years, a variety of general-purpose and specialized large models have emerged in multiple application scenarios, including the analysis and mining of DNA, RNA, and protein sequences, single-cell expression atlases, structure prediction of biomacromolecules, de novo drug design, and interpretation of biological mechanisms. These models have demonstrated significant potential in the domains of biomedical research and translational applications. This paper aims to provide an overview of the characteristics of biological data and the technical methods used for training biological large models, considering the unique features and research application needs of different types of biological data. Furthermore, it reviews the application progress of existing models in biomedical research and disease diagnosis and treatment, offering new insights for enhancing model capabilities and expanding their application scope.

Atherosclerosis, characterized by excess lipid deposition and chronic inflammation, is the common pathological basis of cardiovascular diseases. Macrophages, as important immune cells, are involved in the entire process of atherosclerosis. Recent studies have shown that macrophage efferocytosis is a homeostatic mechanism responsible for the clearance of dead/apoptotic cells and the resolution of inflammation. In atherosclerosis, the capacity of macrophages to participate in efferocytosis is hampered, resulting in the abnormal accumulation of apoptotic cells and necrotic tissue within the plaques, which leads to the enlargement of necrotic core, increased luminal stenosis, plaque inflammation, and ultimate plaque destabilization or rupture. In this review, we summarized the efferocytic machinery that is normally implicated in cardiovascular physiology and then highlighted the mechanisms by which efferocytosis fails in atherosclerosis, aiming to provide therapeutic approaches for this pathological process.

Bile salts, a class of steroidal biosurfactants, play critical roles in lipid digestion and absorption, as well as the regulation of glycolipid metabolism. Their unique molecular structure confers them intriguing aggregation properties and assembly behaviors, distinct from those of classical surfactants. By forming micelles, they facilitate lipid digestion and maintain metabolic homeostasis. In addition, bile salts enhance drug dissolution and absorption through the formation of phospholipid mixed micelles, leveraging their biocompatibility for widespread use as drug absorption enhancers. However, the structure and assembly mechanism of bile salt micelles remain subjects of ongoing debate. This article introduces the molecular structure and aggregation properties of bile salts, as well as the analytical methods for their micellar structures. It summarizes the research progress on the structures of simple bile salt micelles and mixed micelles, and finally, discusses the physiological significance and potential clinical applications of bile salt micelles. Elucidating the structure of bile salt micelles is not only essential for deepening the understanding of their physiological roles, but also provides a theoretical basis for the prevention and treatment of metabolic diseases (e.g., obesity, cholestasis), and supports their innovative applications in fields such as nanodrug delivery.

Cardiovascular diseases (CVDs) are the leading cause of death among both urban and rural residents in China, which are characterized by an extended disease course, diverse symptoms, and complex etiological factors, posing significant challenges to their diagnosis and management. In recent years, the rapid development of artificial intelligence (AI) technologies has provided unprecedented opportunities for early health management and disease prediction in CVDs. By leveraging deep learning and the intelligent analysis of massive health data, AI technologies can accurately identify the potential risks for CVDs and facilitate personalized health management, effectively reducing their incidence and delaying disease progression. The applications of AI technologies have facilitated the improvement of early health monitoring and CVD prevention, as well as improved the accuracy and effectiveness of diagnostic imaging and surgical interventions. In addition, AI technologies have also been applied in biological big data analysis and new drug development. The purpose of this review is to summarize the current applications of AI technologies in CVDs, exploring their prospects and potential challenges in improving diagnostic and therapeutic efficiency. It is anticipated that AI technologies will play an increasingly critical role in the prevention, diagnosis, and treatment of CVDs, thus promoting the advancement of smart healthcare and precision medicine.

Depression is a serious psychiatric disorder that imposes a heavy burden on patients and society. As a widely consumed beverage, coffee is rich in various bioactive components such as caffeine, chlorogenic acid, and diterpenes. Previous studies have indicated that these components may play a role in the prevention and treatment of depression by inhibiting neuroinflammation, combating oxidative stress, and regulating neurotransmitters. Epidemiological studies have demonstrated a significant association between moderate coffee consumption and a reduced risk of depression. This article systematically reviews the antidepressant mechanisms of coffee's bioactive components and related population-based studies, aiming to provide a scientific reference for rational coffee consumption.

Depression is a psychiatric disorder that profoundly affects the psychological and physiological health of patients, imposing substantial mental and economic burdens on both patients and their families. Although pharmacological treatments are commonly used in clinical practice, their prolonged treatment duration and significant side effects limit their clinical applicability and effectiveness. Exercise intervention, as a non-pharmacological physical therapy, offers advantages such as high feasibility and minimal side effects, and has been widely used to promote neurological function recovery in patients. From the perspective of exercise intervention alleviating neurological dysfunction in patients with depression, this article reviews the direct and indirect mechanisms of exercise intervention in the prevention and treatment of depression, focusing on aspects such as promoting neuronal protection and regeneration, regulating the expression of neurotrophic factors, and modulating signal transmission between neurons. The aim is to provide a scientific reference for clarifying the mechanisms by which exercise therapy exerts its antidepressant effects.

Tumor-associated macrophages (TAMs) are highly plastic innate immune cells in the tumor microenvironment of lung cancer and other solid tumors, playing key roles in tumor development, immune resistance, and therapeutic response. With the advent of single-cell sequencing and spatial transcriptomics, the heterogeneity, lineage origins, and dynamic functions of TAMs have been increasingly elucidated, challenging the traditional M1/M2 polarization model. This review summarizes the origins, distribution, polarization states, and metabolic regulation of TAMs in lung cancer, highlighting the impact of lactate-hypoxia axis, lipid metabolism, and cholesterol metabolism on their immunosuppressive functions. We also discuss the roles of TAMs in immune surveillance, tumor proliferation, angiogenesis, metastasis, and immune resistance, with a focus on TREM2+ lipid-associated TAMs in the formation of immune-cold regions and resistance to immune checkpoint inhibitors. Finally, we summarize strategies targeting TAM recruitment, phenotypic reprogramming, metabolic intervention, and combination immunotherapy, and propose personalized interventions based on TAM heterogeneity, providing a theoretical basis for optimizing lung cancer immunotherapy.

Fragment crystallizable γ receptors (FcγRs) are receptors for immunoglobulin G (IgG). Most of them are expressed on the surface of immune cells, and exert relevant biological functions by binding to the Fc region of IgG to form immune complexes. FcγRs are classified into activating and inhibitory types, which exert similar or opposite functions in different cells. In cardiovascular disease research, multiple studies have found that FcγRs expressed on immune and innate cells participate in the occurrence and development of cardiovascular-related diseases such as myocardial infarction, atherosclerosis, and hypertension by activating cell signaling and stimulating the secretion of different cytokines. This article reviews the classification and functions of FcγRs, as well as the research progress on FcγRs in cardiovascular diseases, with the aim of providing new ideas and methods for the prevention and treatment of cardiovascular diseases.

The nucleus reuniens is the largest nucleus in the midline of the thalamus, with extensive afferent inputs and relatively limited efferent outputs. Functionally, this nucleus serves as a pivotal hub connecting the medial prefrontal cortex with the hippocampus, playing significant roles in spatial learning and memory, recognition memory, and fear memory. In addition to these basic physiological functions, recent research has demonstrated the involvement of the nucleus reuniens in various neurological disorders, such as schizophrenia, epilepsy, Alzheimer's disease, depression, and anxiety. This review summarizes the evidence on the role of the nucleus reuniens in the progression of these disorders, aiming to elucidate novel pathophysiological mechanisms underlying the onset and development of brain disorders, and to provide insights for both basic and clinical research.

Thymosin beta-4 (Tβ4), a ubiquitously expressed peptide in mammalian tissues and cells, exerts diverse biological effects in the cardiovascular system. Tβ4 regulates cardiac and vascular development during embryogenesis, maintains stemness characteristics and cellular activity of stem/progenitor cells, induces angiogenesis and vascular maturation, and stabilizes vascular integrity.Exogenous Tβ4 supplementation can regulate immune responses, reduce inflammation, inhibit tissue fibrosis, activate and mobilize myocardial/endothelial progenitor cells for cardiovascular regeneration and repair.These mechanisms collectively enhance functional recovery in ischemic hearts, demonstrating Tβ4's dual regulatory roles in both cardiac and vascular systems. Currently, Tβ4 has entered clinical trials for patients with ST-segment elevation myocardial infarction (STEMI), highlighting its therapeutic potential in ischemic diseases. This review summarizes the structural features and biological functions of Tβ4, focusing on its roles in cardiovascular development and injury repair. We further elucidate its cardioprotective mechanisms to provide a theoretical foundation for advancing Tβ4-based therapeutic strategies.

Autoimmune diseases are characterized by systemic or organ-specific damage mediated by autoimmune responses, which occur when the immune system recognizes and attacks self-antigens. Recent studies indicate a rising incidence of autoimmune diseases and a significant correlation between these diseases and intestinal barrier dysfunction. The intestinal mucosal immune system plays an essential role in maintaining intestinal barrier function and immune tolerance. Dysregulation of this system is implicated in the development of autoimmune intestinal diseases, including inflammatory bowel disease (IBD) and celiac disease, as well as extraintestinal autoimmune diseases, such as systemic lupus erythematosus (SLE) and psoriasis. This review summarizes the composition of the intestinal mucosal immune system and its interactions with various organs, including the gut-liver,gut-kidney,and gut-brain axes,along with their mechanistic roles in autoimmune diseases. It elucidates the mechanisms underlying disorders of intestinal mucosal immunity in autoimmune diseases and highlights recent research advances, providing a reference for developing novel treatment strategies targeting intestinal mucosal immunity for autoimmune diseases.

Coffee, as a globally prevalent beverage, has garnered considerable research attention regarding its association with liver health. Drawing upon recent domestic and international research, this article systematically reviews the preventive and protective effects of coffee consumption on chronic liver diseases. Specifically, it focuses on the protective roles of coffee in diseases such as metabolic dysfunction-associated fatty liver disease (MAFLD), liver cancer, and other chronic liver diseases, as well as the underlying molecular mechanisms. Evidence indicates that moderate coffee intake enhances liver function and health primarily via anti-inflammatory, antioxidant, and metabolic regulatory pathways. Notably, these effects exhibit variations across genders and populations. By integrating clinical evidence with mechanistic research, this review provides a theoretical basis and reference for understanding the role of coffee in chronic liver diseases, and offers scientific recommendations for coffee consumption.