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.

Catestatin, a multifunctional neuroendocrine peptide derived from chromogranin A, is widely expressed in the nervous, endocrine, immune, and cardiovascular systems. Catestatin can bind to nicotinic acetylcholine receptors, activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt),mitogen-activated protein kinase/extracellular signal-regulated kinase(MAPK/ERK), toll-like receptor 4/p38 mitogen-activated protein kinase (TLR4/p38 MAPK), and Notch1 signaling pathways, exerting various biological effects such as antioxidation, promotion of angiogenesis, regulation of immune homeostasis, and modulation of glucose and lipid metabolism. Recent studies have shown that catestatin is involved in the pathophysiological processes of several diseases, including hypertension, atherosclerosis, inflammatory bowel disease, diabetes, and preeclampsia. This review focuses on recent research progress on the origin, structure, receptors, associated signaling pathways, biological effects, and pathophysiological significance of catestatin, with the aim of providing a theoretical basis for further mechanistic research and potential clinical applications of catestatin.

Inflammation is a protective mechanism of the body in response to harmful stimuli. However, persistent inflammation and excessive secretion of inflammatory mediators may lead to chronic inflammation, resulting in dysfunction of cells, tissues, or organs. The vagus nerve isone of the core components in neuro-immune regulation. In recent years, studies have shown that the vagus nerve regulates inflammatory responses, especially anti-inflammatory effects, through multiple pathways, including the cholinergic anti-inflammatory pathway, non-cholinergic anti-inflammatory pathway, and the inflammatory reflex. This review focuses on the core mechanisms underlying the anti-inflammatory effects of the vagus nerve and its clinical applications in autoimmune diseases, infectious diseases, metabolic diseases, and neurological disorders, aiming to provide new insights into clinical anti-inflammatory therapy.

Alzheimer's disease(AD)is a neurodegenerative disease characterized by progressive cognitive dysfunction, with its pathogenesis closely associated with mitochondrial dysfunction. The PINK1/Parkin signaling pathway, as a core regulator of mitophagy, plays a key role in clearing damaged mitochondria and maintaining neuronal homeostasis. While dysfunction of this pathway in Parkinson's disease is mainly attributable to genetic mutations,in AD,it is not a primary cause but rather a secondary consequence of core pathological processes such as abnormal amyloid β-protein (Aβ)deposition and tau protein hyperphosphorylation. These pathological changes can lead to impaired function of the PINK1/Parkin pathway, which in turn triggers mitophagy deficits, creating a vicious cycle of neurodegeneration. PINK1 can activate the mitophagy program by phosphorylating Parkin proteins and ubiquitin molecules, a process that is significantly inhibited in AD. Crucially, the abnormal deposition of Aβ and pathological changes of tau in AD not only inhibit the PINK1/Parkin pathway, but also their own production and toxic effects are regulated by this pathway, forming a complex AD-specific bidirectional interactive network, which is significantly different from the pathophysiological mechanism of Parkinson's disease. Notably, pharmacological interventions aimed at activating the PINK1/Parkin pathway have shown potential in improving AD pathology and cognitive function in animal models. In this review, we systematically elucidate the molecular mechanisms and therapeutic implications of PINK1/Parkin-mediated mitophagy in AD, providing a crucial theoretical basis for the development of novel neuroprotective strategies.

Sialic acid-binding immunoglobulin-like lectin 15 (Siglec-15) is a member of the Siglec family and functions as an immunosuppressive receptor within the Siglecs superfamily. In recent years, its role in tumor immunity has attracted increasing attention. By modulating the immune microenvironment, Siglec-15 contributes to tumor progression and prognosis,emerging as a novel target for cancer immunotherapy. Immunotherapy for gastrointestinal tumors has become a pivotal treatment approach following surgery, chemotherapy, radiotherapy, and targeted therapy. While PD-1/PD-L1 and CTLA-4 inhibitors have shown efficacy in some patients, challenges such as drug resistance and biomarker identification remain. This review systematically summarizes recent advances in understanding the relationship between Siglec-15 and gastrointestinal tumor immunity, covering its biological characteristics, expression patterns in gastrointestinal cancers, immunomodulatory mechanisms, and potential therapeutic strategies targeting Siglec-15. These findings may provide new insights and approaches for immunotherapy in gastrointestinal malignancies.

Human immunodeficiency virus type 1 (HIV-1) is the main pathogen of acquired immune deficiency syndrome (AIDS), which can cause a variety of opportunistic infections,tumorigenesis, and eventually death. Studies have indicated that exosomes play a crucial role during the progression of persistent HIV-1 infection, acting as key mediators of intercellular communication. This review focuses on the involvement of exosomes derived from dendritic cells,T cells, and semen in HIV-1 infection. It also elucidates the role of blood-derived exosome contents, specifically microRNAs (miRNAs),which not only serve as biomarkers but also participate in the HIV-1 infection process. Furthermore,blood-derived exosomes mediate HIV-1-associated chronic inflammation, thereby contributing to the infection process. This review also discusses the mechanisms by which brain-derived exosomes induce HIV-1-associated neurocognitive disorders, as well as their therapeutic implications, and the role of T cell-derived exosomes in promoting the occurrence and development of HIV-1-associated malignancies. This article elaborates on the mechanisms by which exosomes from diverse origins contribute to the occurrence, development, and outcomes of HIV-1 infection, with the aim of providing new insights for early screening and therapeutic intervention of HIV-1 infection.

The intervertebral disc consists of the nucleus pulposus, annulus fibrosus, and cartilage endplates, and plays a crucial role in maintaining the normal physiological function of the spine. Intervertebral disc degeneration (IDD) is the primary pathological basis for spinal degenerative diseases such as low back pain, imposing a significant health burden on individuals. However, the molecular mechanisms underlying IDD remain poorly understood, leading to a lack of effective targeted intervention strategies. The RAS homolog family member A (RhoA)/Rho-associated protein kinase (ROCK) signaling pathway is a classical pathway regulating cell contraction, migration, and growth. Upon activation, it participates in regulating cytoskeletal remodeling, extracellular matrix metabolism, circadian rhythms, cellular phenotype changes, cellular senescence, and cell death, thereby influencing the pathological progression of IDD. Elucidating the role of the RhoA/ROCK signaling pathway in IDD not only provides insight into the molecular mechanisms of disease development, but also offers a theoretical basis for developing therapeutic strategies targeting this pathway.

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.

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.

Coffee, a globally consumed beverage, contains multiple bioactive compounds, including caffeine, trigonelline, polyphenols, and diterpenes. These bioactive constituents exhibit potential anti-colorectal cancer effects through multi-target mechanisms, including suppression of the Wnt/β-catenin pathway, modulation of oxidative stress, activation of immune responses, and promotion of cancer cell apoptosis, while inhibiting growth and migration of colorectal cancer cells. Research indicates that coffee consumption significantly reduces mortality and improves prognosis for patients with advanced colorectal cancer. This article systematically reviews the biological effects and clinical relevance of coffee' s primary constituents, aiming to provide a theoretical basis for dietary interventions in the prevention and treatment of colorectal cancer.

v-ets erythroblastosis virus E26 oncogene homolog 2 (ETS2) is a transcription factor that plays a crucial role in regulating normal physiological processes such as growth and development, as well as in tumorigenesis. Moreover, aberrant expression and activity of ETS2 are closely associated with the pathogenesis and progression of cardiovascular diseases. This review summarizes the latest advances in ETS2 research within the context of cardiovascular diseases, providing new insights for future investigations into the pathogenesis of cardiovascular diseases and the development of therapeutic targets.

Chaperone-mediated autophagy (CMA) is a highly selective intracellular degradation pathway that plays a pivotal role in maintaining cellular homeostasis, as well as in the onset and progression of disease. CMA significantly influences cellular homeostasis by regulating protein homeostasis, mediating stress responses, modulating the cell cycle, contributing to the regulation of ferroptosis, and sustaining mitochondrial function. Dysfunction of CMA is closely associated with the development of numerous diseases. In recent years, the role of CMA in pulmonary diseases has received increasing attention. This review summarizes the latest research on the role and mechanisms of CMA in lung cancer, chronic obstructive pulmonary disease and acute lung injury, with the aim of providing novel insights into the treatment of pulmonary disorders.

Gastric cancer, as a highly prevalent malignant tumor of the digestive system worldwide, demands the identification of new molecular targets given its high recurrence rate and poor prognosis.E2F Transcription Factor 1(E2F1), a core transcription factor of cell cycle regulation, has been shown to exert important roles in gastric cancer via its aberrant expression and functional alterations. Several tissue microarray and database studies have shown that E2F1 is highly expressed in gastric cancer tissues, with its expression level varying across different stages and pathological subtypes. Moreover, its expression significantly correlates with the degree of tumor differentiation, depth of invasion, and patient survival outcomes. Mechanistically, E2F1 not only promotes cell cycle progression by regulating downstream targets such as DNA topoisomerase II alpha, cyclin-dependent kinase 6 and cell division cycle 25B, but also participates in apoptosis regulation, epithelial-mesenchymal transition, stemness maintenance, and immunosuppressive microenvironment construction. Especially in maintaining tumor stemness and driving chemoresistance, E2F1 interacts with various non-coding RNAs to enhance the invasiveness of gastric cancer cells. Further studies have revealed that high E2F1 expression is associated with increased infiltration of immunosuppressive cells, including regulatory T cells, M2-polarized tumor-associated macrophages, and exhausted CD8+ T cells, highlighting its pivotal role in facilitating immune evasion. In conclusion, E2F1 plays a multidimensional regulatory role in the development of gastric cancer, endowing it with potential diagnostic, prognostic and therapeutic intervention value, and provides a theoretical basis for the subsequent targeted therapy and combined immunotherapy.