The aorta is one of the most important arteries in the human body. Although its basic vascular functions have been extensively studied, its multiple physiological roles as an independent organ have often been overlooked. Recent studies have shown that the aorta not only plays a central role in blood pressure maintenance, but also participates in key physiological processes such as metabolism, endocrinology, nervous system regulation, and immune stress. The unique structure and function of the aorta endow it with significant roles in a variety of physiological and pathological states. This article reviews the importance of the aorta as an independent organ and discusses its structural and functional uniqueness. Emphasis is placed on the metabolic and endocrine regulatory functions of aortic endothelial cells and smooth muscle cells, as well as the role of the aorta in neuroregulation and immune stress. The discussion of these research advances provides new perspectives for an in-depth understanding of the physiological and pathological functions of the aorta and offers potential research directions for future studies.

Tumor immunotherapy has achieved impressive therapeutic effects in clinical practice and has attracted increasing attention. Among them, chimeric antigen receptor T (CAR-T) cell therapy has made breakthrough progress in the treatment of hematological malignancies. However, with prolonged exposure to tumor antigens, CAR-T cells may become exhausted in vivo. The exhaustion of CAR-T cells can lead to poor treatment efficacy or tumor recurrence. The mechanism of CAR-T cell exhaustion involves a series of processes, such as the expression of exhaustion-associated transcription factors, the role of the immunosuppressive tumor microenvironment, and the influence of CAR structure itself. Here, we summarize the process and underlying mechanisms of CAR-T cell exhaustion, as well as potential solutions to improve T cell exhaustion and enhance the efficacy of CAR-T cell therapy, with the aim of expanding the application of CAR-T cell therapy in tumor treatment.

Circadian rhythm is a biological process that operates on an approximately 24-hour cycle, encompassing various physiological functions including blood pressure, heart rate, and body temperature. The normal circadian rhythm of blood pressure typically exhibits a characteristic “two-peak and one-valley” pattern, which is regulated by a combination of exogenous factors, including light exposure, exercise, and diet, as well as endogenous factors such as the autonomic nervous system, stress hormones, and clock genes. In recent years, lifestyle factors such as nocturnal light exposure, shift work, and jet lag have increasingly led to circadian rhythm disruption. The normal circadian rhythm of blood pressure is also often affected, contributing to circadian rhythm disorders of blood pressure. Numerous studies indicate that exercise can prevent cardiovascular diseases such as hypertension and heart failure, serving as an important non-pharmacological strategy to mitigate the disruptions in the circadian rhythm of blood pressure. Therefore, this review will take the factors influencing the circadian rhythm of blood pressure as a starting point, aiming to clarify the possible mechanisms through which exercise participates in regulating the blood pressure circadian rhythm, and to provide a theoretical basis for improving the circadian rhythm disorders of blood pressure through exercise.

Titin (TTN), the largest protein by molecular weight in humans, extends beyond its roles in providing structural stability to the sarcomere and storing elastic potential energy. It also plays a crucial regulatory role in muscle hypertrophy and protein quality control. The protein complex encompassing the Z-disk, I-band, and M-line regions of TTN acts as a mechanosensor, dynamically modulating the transduction of myocellular hypertrophic signaling in response to mechanical tension. TTN induces skeletal muscle remodeling after exercise, mediating the repair and degradation of damaged TTN through protein protection and quality control mechanisms. Under appropriate mechanical stimulation, the TTN mechanosensory complex is activated, thereby triggering a series of hypertrophic responses. Conversely, following overload exercise, severely damaged TTN promotes its degradation through interactions of T-cap with MDM2, the proximal Ig region with calpain 1, and the N2A and M-line regions with calpain 3, as well as engagement of the MuRF1 binding site within the M-line domain. In this article, we delve into the role of the cytoskeletal protein TTN as a central signaling hub for skeletal muscle remodeling. Initially, the basic structure of TTN is elucidated, followed by an in-depth analysis of the mechanisms by which different regions contribute to muscle hypertrophy and protein quality control.

Myokines exert a significant beneficial effect on cardiovascular and metabolic diseases. As a recently identified myokine, myonectin is closely associated with various cardiovascular and metabolic diseases, such as coronary heart disease, diabetes, and obesity. This article reviews the biological characteristics of myonectin, its role in the occurrence and development of cardiovascular and metabolic diseases, and its potential mechanisms of action, aiming to provide new targets and strategies for the prevention and treatment of cardiovascular and metabolic diseases.

The incidence and mortality of various tumors have been increasing, and the search for novel anti-tumor targets is one of the major research directions for anti-tumor drug development. Transient receptor potential canonical (TRPC) channels are a class of critical non-selective cation channels permeable to sodium (Na+ ), calcium (Ca2+ ), and other cations located on the cell membrane, which are widely distributed in vivo and participate in a variety of physiological and pathological processes. Studies have shown that the protein and mRNA levels of TRPCs are abnormally overexpressed in various tumor cells, which can promote tumor proliferation by increasing the intracellular Ca2+ concentration of tumor cells. Since TRPC receptors are located on the cell surface, ion channel-targeted drugs do not need to enter the cell, making them ideal therapeutic targets. Ca2+ , as one of the most essential intracellular messengers, plays a critical role in regulating cell growth and death, as well as tumor cell proliferation and apoptosis. Ca2+-permeable TRPC channels play a crucial role in tumor development, making them prognostic markers and potential therapeutic targets for malignant tumors. Targeting TRPC channels to regulate intracellular Ca2+ concentration and, in turn, modulate downstream signaling pathways is a novel approach to inhibiting tumor cell proliferation. This review summarizes the effects and mechanisms of TRPCs on tumorigenesis and development, and focuses on the potential of the extracellular small molecule binding pockets of the TRPC family as targets for anti-tumor small molecule compounds.

Parkinson's disease (PD) is a chronic, progressive neurodegenerative disorder characterized by classic clinical features including motor symptoms such as tremor, muscle rigidity, bradykinesia, and abnormal posture and gait, as well as a variety of non-motor symptoms. Mitochondrial dysfunction plays a crucial role in the pathogenesis of PD, propelling genes associated with mitochondrial function to the forefront of current research endeavors. Some gene mutations are closely related to the pathogenesis of PD. Mitochondrial-related PD pathogenic genes include genes involved in mitochondrial dynamics, mitochondrial DNA homeostasis, mitochondrial protein translation, the mitochondrial respiratory chain, and mitochondrial metabolism, participating in the regulation of mitochondrial function and mitochondrial quality control, ultimately leading to structural and functional abnormalities in mitochondria. This article provides an overview of the mitochondrial-related PD pathogenic genes that are directly or indirectly associated with the onset and development of PD. Through in-depth studies of the functions and mechanisms of these genes, it is hoped that better therapeutic methods and prevention strategies for PD can be identified.

Methyltransferase-like 8 (METTL8) is a member of the methyltransferase-like protein (METTL) family, which typically utilizes S-adenosylmethionine (SAM) as a substrate to catalyze methylation. 3-methylcytidine (m3C) is a type of methylation that occurs at the third nitrogen atom of the cytosine base in RNA, playing a wide-ranging role in maintaining RNA secondary structure, stability, and function. METTL8 is currently the only enzyme known to regulate m3C modification in both messenger ribonucleic acid (mRNA) and transfer ribonucleic acid (tRNA). Additionally, METTL8 is closely associated with processes such as embryonic stem cell differentiation, skeletal muscle gene regulation, and tumor proliferation. Given the significant role of METTL8, this article focuses on the structural composition, functional characteristics, and research progress associated with METTL8, aiming to provide insights for further investigation into its biological functions.

Acyl-coenzyme A binding domain containing 3 (ACBD3) is a scaffold protein of the Golgi apparatus that participates in various protein-protein interactions. ACBD3 plays a wide range of biological roles in cellular function and signal transduction. It is involved in mitochondrial cholesterol transport and steroid synthesis, regulating processes such as pathogen replication, cell apoptosis, and neurogenesis. Furthermore, ACBD3 plays crucial roles in the occurrence and development of diseases, such as tumors and Huntington' s disease. In this article, we review the research progress on the structural characteristics and physiological functions of ACBD3.

Ferroptosis is a form of programmed cell death associated with abnormal iron metabolism and excessive accumulation of lipid peroxides, characterized by unique biological processes and pathophysiological features. Lipid peroxidation represents the most fundamental mechanism underlying ferroptosis. Increasing evidence indicates that ferroptosis plays significant regulatory roles in the onset, development, and treatment of tumors.Induction of ferroptosis in tumor cells can effectively inhibit tumor growth and metastasis, and improve the therapeutic sensitivity of anti-tumor drugs. This article reviews the mechanisms by which lipid metabolic processes, such as the synthesis and remodeling of phospholipids,the storage and release of phospholipids,as well as the uptake and oxidation of fatty acids,regulate ferroptosis.It summarizes the effects of lipid metabolism-associated signaling pathways on ferroptosis and targeted therapeutic strategies, aiming to provide new insights for ferroptosis-associated basic research and clinical tumor therapy.

The intestinal mucosal barrier is the first barrier between the intestine and the external environment, preventing harmful substances and pathogens from entering the internal environment and maintaining intestinal homeostasis. Bile acids, synthesized from cholesterol in the liver and subsequently converted into secondary bile acids by gut microbiota, interact with bile acid receptors and the gut microbiome, playing a key role in maintaining the homeostasis of the intestinal mucosal barrier. This review will elaborate on the role of bile acids and bile acid metabolism in the structure of the intestinal mucosal barrier, as well as the relationship between bile acids and intestinal diseases, aiming to provide insights for future strategies in the prevention and treatment of intestinal barrier dysfunction and associated intestinal diseases.

Diabetic kidney disease(DKD)is a severe microvascular complication of diabetes mellitus, representing the most common form of chronic kidney disease and a major cause of end-stage renal disease. Currently, available treatment options have notable limitations, including poor bioavailability, hepatorenal toxicity of oral medica-tions, and a lack of precise targeting. In recent years, nano-drug delivery systems (NDDS) have demonstrated significant potential in the treatment of kidney diseases. Nanocarriers are capable of targeting drugs to specific areas, addressing the issue of inadequate drug delivery to particular sites, and enhancing therapeutic efficacy. This article reviews the pathogenesis of DKD and the limitations of current treatment methods, while focusing on the application of NDDS in treating DKD. Finally, it presents the challenges and new visions for the future development of nanoplatforms, providing insights for achieving efficient targeted therapy for the kidney diseases.

The repair and regeneration of bone tissue defects is a complex and slow pathophysiological process,representing a significant challenge in oral clinical treatment. Hypoxia leads to an inadequate blood supply to injured bone tissue,significantly impairing the repair and regeneration of bone tissue defects.Magnesium and magnesium alloys, as novel types of degradable and absorbable materials for bone tissue engineering implants,release magnesium ions under hypoxic conditions. These magnesium ions can activate cell signaling pathways related to hypoxia-inducible factors, promoting angiogenesis,preserving the osteogenic function of bone cells,and facilitating the repair and regeneration of injured bone tissue.Accordingly,this article reviews the factors influencing bone tissue regeneration under hypoxic environments and current state of research on the mechanisms by which magnesium ions promote bone regeneration,aiming to lay a foundation for the subsequent development of various medical magnesium alloy biomaterials that facilitate the repair of bone tissue defects.

Fractures can lead to pain, limited mobility, and a decreased quality of life. Treatment typically involves surgical or conservative approaches, often accompanied by complications. Stem cell-derived exosomes (EXOs), characterized by excellent biocompatibility, low immunogenicity, intrinsic stability, and targeting ability, have emerged as a current research hotspot. Exosomes hold certain advantages in promoting fracture healing; they can regulate the functions of osteoblasts and osteoclasts, angiogenesis, and cartilage regeneration, which may improve clinical treatment outcomes and reduce the incidence of fracture complications. In this article, we review the research progress on exosomes derived from human umbilical cord mesenchymal stem cells (HUC-MSCs) in promoting fracture healing, exploring the critical role of HUC-MSC-derived exosomes in this process.