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.

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。 。

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.

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.

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.

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.

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.

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.

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.

Caffeine is a well-established ergogenic aid in the field of sports science, with a robust body of research confirming its positive effects on exercise performance. Current evidence indicates that caffeine intake improves performance across various exercise modalities, including reaction time tasks, short-term high-intensity strength training, and endurance aerobic exercise. Empirical data suggest that an intake of 2-4 cups of coffee (equivalent to 3-6 mg/kg of caffeine) approximately 60 minutes before exercise can optimize these ergogenic benefits. However, individual metabolic sensitivity and physiological characteristics must be considered for personalized recommendations. This review systematically summarizes the effects of caffeine intake on various types of exercise performance and elucidates the underlying biological mechanisms. It aims to provide a theoretical basis for future research on the synergistic mechanisms of coffee and exercise, adaptive changes resulting from long-term consumption, and individual differences caused by genetic polymorphisms, thereby facilitating the precise application of caffeine in both competitive sports and public health.

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.

With the accelerating aging of the global population, osteoporosis has emerged as a major public health challenge. As one of the most widely consumed beverages, the relationship between coffee intake and osteoporosis remains controversial. Previous research has often treated coffee as a single entity, neglecting the complexity of its chemical composition. Based on the principle of bone metabolic homeostasis, this review systematically elaborates on the dual regulatory effects of its key constituents—coffee polyphenols and caffeine—on osteoporosis from a compositional perspective. Polyphenols exert protective effects on bone through mechanisms such as antioxidation, anti-inflammation, and modulation of the gut-bone axis, whereas caffeine promotes bone resorption by disrupting calcium homeostasis and potentially activating osteoclasts. By synthesizing the latest evidence and analyzing sources of heterogeneity across studies, this review concludes that the net impact of coffee on bone health is determined by the balance between these components, total daily intake, and individual physiological conditions. This work aims to provide a scientific basis for personalized dietary recommendations regarding coffee consumption for different populations and to inform the development of precise dietary guidance systems.

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 circadian rhythm is an endogenous biological oscillation with a 24-hour period. Under normal physiological conditions, the circadian rhythm of blood pressure exhibits a diurnal variation characterized by a two-peak-one-trough pattern, with higher levels during the day and lower levels at night. Extensive studies have demonstrated that the circadian regulation of blood pressure depends on the precise integrative functions of the cardiovascular centers. The brainstem and hypothalamus modulate the dynamic balance between the sympathetic and parasympathetic activities via neurotransmitters, endocrine signals, and other pathways, thereby maintaining physiological fluctuations of blood pressure. Under pathological conditions, dysregulation of cardiovascular centers can lead to abnormal circadian rhythm of blood pressure, which is closely associated with cardiovascular diseases such as hypertension. Therefore, this review systematically examines the role and molecular mechanisms of cardiovascular center in regulating blood pressure circadian rhythms, providing a theoretical basis for revealing the pathogenesis of abnormal blood pressure rhythms and developing targeted therapies.

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.

Mitochondria are essential organelles that execute and coordinate various metabolic processes in cells. Mitochondrial dysfunction significantly affects cellular health and leads to a variety of diseases. The maintenance of mitochondrial health depends on dynamic changes in the mitochondrial membrane network and effective mitochondrial quality control mechanisms. Increasing evidence suggests that mitochondria-associated endoplasmic reticulum membranes (MAMs), formed between mitochondria and the endoplasmic reticulum, play a crucial role in regulating mitochondrial quality control. This article reviews the research progress of MAMs in regulating mitochondrial quality control, revealing that the structural and functional changes of MAMs are closely related to disorders of mitochondrial quality control, providing new perspectives and potential therapeutic targets for understanding and treating associated diseases. Future studies need to further clarify the specific regulatory mechanisms of MAMs in different diseases and develop effective intervention strategies, with the aim of achieving precise treatment of associated diseases in clinical practice.

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.

As a vital locomotor organ in the human body, skeletal muscle plays a crucial role in sustaining life, and the maintenance of its homeostasis is fundamental to the proper execution of various physiological functions. Exercise influences skeletal muscle through multiple mechanisms, notably by regulating muscle protein synthesis and degradation, and by modulating metabolic balance, thereby contributing significantly to the maintenance of skeletal muscle homeostasis. However, the specific mechanisms by which exercise maintains skeletal muscle homeostasis have not yet been fully elucidated. Notably, high-intensity exercise promotes glycolysis within skeletal muscle, resulting in lactate production. Recent studies, however, have revealed a new perspective: lactate can serve as a donor for protein lactylation, modifying both histone and non-histone proteins. This modification plays a critical role in various physiological activities within skeletal muscle. In this context, this review summarizes recent research on lactate and lactylation, exploring their roles and potential mechanisms in maintaining skeletal muscle homeostasis, with the aim of providing novel insights and therapeutic targets for preventing and treating skeletal muscle-associated diseases through exercise.

Tumor development is closely related to the aberrant post-transcriptional regulation mediated by RNA-binding proteins (RBPs), which play a key role in tumor progression by regulating mRNA splicing, stability, and translation. This review systematically investigates the molecular mechanisms underlying the abnormal expression or dysfunction of RBPs during tumor development, the molecular basis of RBPs in promoting tumor progression through regulating tumor-associated signalling pathways, and the roles of RBPs in malignant transformation and therapeutic resistance, aiming to provide an important theoretical basis for developing anti-tumor therapies targeting RBPs.