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  • CHEN Qi, CHEN Shi-Cheng, LIU Yu-Chen, WANG Cui-Tong, CHENG Bin, LAN Ke△
    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.
  • ZHU Li, XU Yu-Shan△
    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.
  • ZHANG Ying-Ge1, 2, ZHANG Ya-Rong2, △ , WANG Jing2
    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.
  • ZHU Ming-Yue1, QIAO Xue-Song2, △ , NIU Yan-Mei1, △
    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.
  • WANG Zi-Hang1 , PU Zi-Jie1, CAI Liang-Liang1, SHEN Min1, △ , QIAN Li1, 2, △
    Histone methylation, a critical epigenetic modification, is meticulously regulated by specific methyltransferases and demethylases. Changes in the methylation levels at specific histone sites play a key role in gene transcription regulation, inflammatory responses, and disease progression. Alternations in the levels of histone methylation and the expression of associated modifying enzymes contribute significantly to the pathogenesis of chronic liver diseases, including viral hepatitis, metabolic-associated fatty liver disease, liver fibrosis, and hepatocellular carcinoma. This review summarizes recent research advances regarding histone methylation and inhibitors of associated modifying enzymes in the context of chronic liver diseases, aiming to provide a reference for the translational application of basic research into clinical therapies for these conditions.
  • CHEN Zhe1, LIAO Zhao-Hong1, LIU De-Liang2, △
    Ferroptosis is an emerging form of iron-dependent cell death regulated by lipid peroxidation. It has revealed novel mechanisms underlying the onset and progression of disease across various fields such as cell biology and pathology, providing fresh insights and promising therapeutic targets for the treatment of numerous intractable diseases. The intestinal microbiota constitutes the largest microecological system within the human body and plays a crucial role in maintaining host health by regulating various physiological processes, including metabolism, immunity, and neural activity. In recent years, accumulating evidence has emphasized a close relationship between intestinal microbiota and ferroptosis in various pathological conditions. This article reviews the latest research on the mechanisms of ferroptosis and its regulation by intestinal microbiota, aiming to provide a comprehensive understanding of the role of ferroptosis in diseases, and to offer both a theoretical foundation and practical guidance for the development of novel therapeutic strategies based on regulating intestinal microbiota.
  • XIONG Wei1, CHAI Xing-Xing2, LI Li-Li2, △
    Parkinson's disease (PD), the second most common neurodegenerative disorder worldwide, is pathologically characterized by the progressive loss of nigral dopaminergic neurons, leading to motor dysfunction and other symptoms. Astaxanthin (AST), a potent natural antioxidant, possesses both antioxidative and anti-inflammatory properties and is capable of crossing the blood-brain barrier. Studies have demonstrated that AST reduces oxidative stress-induced neuronal damage, decreases the release of inflammatory factors, and inhibits apoptosis by modulating various signaling pathways, thereby exerting neuroprotective effects and showing potential value in the prevention and treatment of PD. This article explores the protective mechanisms of AST on nigral dopaminergic neurons in the context of PD, with the aim of providing references and guidance for clinical treatment and the development of novel drugs for PD.
  • Physiological Science and Clinical Medicine
  • Physiological Science and Clinical Medicine
    WANG Qin-Shuo1, ZHAO Xin-Hui2, WU Cong-Ying3, △, Yang Yang2, △
    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.
  • Physiological Science and Clinical Medicine
    LUO Dan-Ni1, LI Shu-Yan2, △
    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.
  • Physiological Science and Clinical Medicine
    CHENG An-Qi1, 2, ZHAO Yu-Yu1, 2, LI Xin1, 2, LI Su-Xia2, △
    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.
  • Review on the Nobel Prize
  • Review on the Nobel Prize
    Huang Jing, Qiu Xiao-Yan
  • Monograph
  • Monograph
    LIU Hui-Jin, WENG Zhi-Qing, CHEN Dong-Kun, WU Fei, JIA Jun, WANG Ke△
    Timely and appropriate motor inhibition is essential for daily life. Response inhibition (RI) is a crucial component of the brain's inhibitory control functions, which can be categorized into reactive and proactive inhibition. Classic paradigms, such as the Go/No-Go and Stop-signal tasks, are primary methods for investigating the mechanisms of response inhibition. The frontal lobe-basal ganglia circuit plays a central role in regulating response inhibition, in which the hyper-direct pathway in the basal ganglia mediates reactive inhibition, exerting immediate and global effects, whereas the indirect pathways mediate proactive inhibition, exerting slower and more selective effects. Lesions to this neural circuit often result in motor control deficits, which are closely associated with clinical symptoms such as impulsivity, tics, and freezing. The review aims to provide a comprehensive overview of current research on the neural circuits involved in response inhibition, with particular emphasis on the role of the basal ganglia, potentially offering novel insights for symptom control and further investigation into clinically relevant diseases.
  • Monograph
    DAI Jia1, 2, MA Jian-Tong1, FU Kai-Yue3, YUAN Xin-Yi3, YU Lei2, △ , CUI Hong-Wei4
    Lung cancer is the leading cause of cancer-related deaths worldwide,with a complex pathogenesis and significant challenges in clinical treatment.In recent years, the regulatory role of deubiquitinating enzymes in tumorigenesis and progression has garnered increasing attention. As the largest subfamily of deubiquitinating enzymes, ubiquitin-specific proteases (USPs) exert multidimensional regulatory effects on the initiation and progression of lung cancer by precisely modulating the stability of key signaling pathway proteins.This review systematically summarizes the molecular mechanisms by which the USPs family regulates the lung cancer cell cycle progression, proliferation,apoptosis evasion,invasion and metastasis, immune microenvironment remodeling, and therapy resistance. It highlights the molecular networks of key members, such as USP7, USP9X, and USP22, in modulating lung cancer progression through critical signaling pathways, including p53, programmed death ligand 1 (PD-L1), and Wnt/β-catenin. Additionally, the review comprehensively analyzes the latest advances in the development of small-molecule inhibitors targeting USPs and explores their potential applications in precision therapy for lung cancer, aiming to provide a theoretical foundation for novel diagnostic and therapeutic strategies.
  • Monograph
    HUANG Xue-Mei1, 2, NIE Ya-Dan1, 2, WANG Hai-Xia1, 2, HE Yi1, 2, LUO Yan-Ting1, 2, △
    As resident immune cells of the central nervous system, microglia play critical roles in immune surveillance, immune responses, as well as in the development and maintenance of the nervous system. Microglia exhibit a high degree of heterogeneity and sensitivity, and research into their complex regulatory mechanisms and diverse functions has become a major focus in brain science. This article provides a comprehensive overview of methods for studying microglial morphology and function based on traditional research models and high-throughput sequencing technologies. It covers in vivo and in vitro models, microscopic imaging and visualization techniques, as well as analysis methods based on sequencing data. The characteristics and application scopes of these approaches are summarized, providing references for future multidimensional investigations into microglial phenotypic changes and functions.
  • Monograph
    CHAI Rui-Qing1, 2, LIANG Ya-Nan2, WANG Rui2, ZHANG Tong-Mei3, ZHAO Xing-Cheng2, △
    Angiogenesis is a key process in both embryonic and postnatal individual development, and its dysregulation is closely associated with various diseases, such as tumors, atherosclerosis, and age-related macular degeneration. Recent studies have shown that angiogenesis exhibits circadian rhythmicity, with BMAL1(brain and muscle Arnt-like 1 protein), a core regulator of the circadian clock, playing a critical role in this process. In this article, we review the role and mechanism of BMAL1 in regulating endothelial cell proliferation and migration, vascular maturation, and vascular homeostasis, providing a foundation for a deeper understanding of the molecular mechanism of angiogenesis and the development of vascular-targeted therapies.
  • Monograph
    WEI Xiao-Nan1, CAI Ya-Hui2, SUN Xiao-Yu2, WANG Shan-Shan1, YANG Yi-Qiong1, LI Yan-Ping1, △
    Silent information regulator 3(SIRT3), a member of the silent information regulator family, primarily regulates mitochondrial metabolism, and plays a critical role in age-related diseases, neurodegenerative disorders, as well as cardiac, hepatic, renal, and metabolic diseases. Notably, in cancer, SIRT3 exhibits both tumor-suppressive and tumor-promoting functions, making it a promising therapeutic target. This review systematically summarizes the complex molecular mechanisms of SIRT3 in tumorigenesis and its roles in various malignant tumors, including colorectal cancer, lung cancer, hepatocellular carcinoma, ovarian cancer, gallbladder cancer,cholangiocarcinoma,and pancreatic cancer. Elucidating the mechanisms of SIRT3 not only contributes to revealing the molecular basis of tumorigenesis, but also holds promise for promoting the development of novel antitumor agents targeting SIRT3, thereby providing new directions for clinical cancer therapy.