Anti-tumor drugs, especially chemotherapy drugs, are among the most widely employed approaches for cancer treatment due to their cost-effectiveness and significant therapeutic efficacy. However, their side effects, particularly cardiotoxicity, significantly limit their clinical application. With advancements in biotechnologies, such as active ingredient extraction and nanomaterials, an increasing number of strategies have been developed to mitigate the cardiotoxicity caused by anti-tumor drugs. This review elucidates the potential mechanisms underlying antitumor drug-induced cardiotoxicity, summarizes current research progress on cardioprotective interventions, and provides insights into potential strategies for achieving safer cancer treatment.

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.

Escherichia coli (E. coli), a prevalent commensal bacterium within the resident gut microbiota, includes pathogenic strains that are a leading cause of infant diarrhea in developing countries. In light of the rising antibiotic resistance associated with diarrhea treatment, conventional antibiotic therapies are encountering increasing challenges, underscoring the urgent need for novel therapeutic strategies. The pathogenicity of E. coli is primarily mediated by virulence factors, which play critical roles in facilitating intestinal adhesion and colonization during the early stages of infection. This article reviews recent research progress on E. coli colonization and infection, including its classification, epidemiology, and molecular mechanisms underlying its pathogenicity. It focuses on analyzing the effects of relevant virulence factors and the DcuSR two-component system on the adhesion and colonization of E. coli. Furthermore, the article delves into the impact of hyaluronic acid (HA) on E. coli infection, offering novel insights into the management of E. coli infections.

Non-coding RNA (ncRNA) is a class of RNA molecules transcribed from the genome that do not encode proteins, encompassing various types such as microRNA (miRNA) and long non-coding RNA (lncRNA). These RNAs play pivotal regulatory roles in gene expression, cellular development, and the onset and progression of diseases, and are considered as novel potential drug targets. Small molecule drugs, as key methods of clinical treatment, exert therapeutic effects by interacting with specific targets and play a crucial role in the treatment of various complex diseases. Leveraging intelligent computing methods to predict the potential associations between ncRNAs and small molecule drugs is of significant importance for developing novel drugs, expanding therapeutic strategies, and elucidating biological mechanisms. This article reviews the research progress on intelligent computing methods for predicting the associations between ncRNAs and small molecule drugs, and provides insights into their future development directions.

Type 2 diabetes mellitus (T2DM) is a heterogeneous metabolic disorder characterized by reduced insulin sensitivity and relative insulin deficiency. Long-term T2DM can cause lesions in multiple organs and tissues, including the central nervous system, potentially inducing cognitive dysfunction, and resulting in increased mortality, which has emerged as a significant public health concern and economic burden in the 21st century. Regular physical exercise plays a crucial role in alleviating the development of cognitive impairment in type 2 diabetes. However, the underlying mechanisms remain unclear. This article reviews the pathogenesis of cognitive impairment in type 2 diabetes, and summarizes the mechanisms by which exercise exerts its beneficial effects, thereby providing new insights for future strategies to alleviate cognitive impairment in diabetes.

Musculoskeletal disorders are common complications of sports injuries and age-related degeneration that negatively affect motor function and quality of life.Therefore,identification and screening of novel intervention targets are crucial for the rehabilitation and treatment of musculoskeletal disorders.Current research has indicated that the mechanosensitive channel Piezo1 regulates the metabolic homeostasis of the musculoskeletal system, including satellite cells, bones,tendons, and intervertebral discs, through multiple signaling cascades and molecular mechanisms. Moreover, Piezo1 is involved in the pathogenesis of musculoskeletal disorders, thereby emerging as a potential target for therapeutic intervention. In this article, we systematically discuss the microstructure, molecular regulatory network, and specific agonists and antagonists of Piezo1, as well as its functional roles in skeletal muscles, bones, tendons, and intervertebral discs, aiming to provide novel intervention targets and a theoretical basis for the rehabilitation and treatment of musculoskeletal disorders.

The incidence of neurodegenerative diseases has been steadily increasing. Exercise has been shown to facilitate communication between skeletal muscle and brain. However, the specific signaling molecules secreted by skeletal muscle during exercise and their roles in muscle-brain crosstalk, particularly in the regulation of neuroplasticity, cognitive function, and neuroprotection, remain unclear. This review explores the roles of exercise-induced, skeletal muscle-derived signaling molecules in muscle-brain crosstalk, with a focus on the mechanisms by which myokines (e.g., BDNF, irisin), metabolic products (e.g., lactate), and other relevant signaling molecules influence neuroplasticity, cognitive function, and neuroprotection. These mechanisms include promoting neuronal survival, synaptic plasticity, and neurogenesis, as well as interacting with neurotransmitters in the brain to exert anti-inflammatory, neuroprotective, and metabolic regulatory effects. Furthermore, myokines play an active role in the prevention and treatment of metabolic diseases such as diabetes and obesity. This article aims to provide scientific evidence for the application of exercise interventions in maintaining brain health and in the prevention and treatment of neurodegenerative diseases.

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.

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.

Multiple myeloma is a progressive neoplastic disease caused by the abnormal proliferation of plasma cells in the bone marrow,which leads to the excessive production of aberrant immunoglobulins. Its pathogenesis is closely associated with the dysregulation of the immune microenvironment. As an incurable hematological malignancy,multiple myeloma currently faces limitations in its treatment options,including drug resistance and disease recurrence,posing a significant threat to patients' well-being and survival.The NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome,a multiprotein complex crucial for intracellular immune regulation,plays a pivotal role in the occurrence,progression,and drug resistance of multiple myeloma. This article systematically summarizes the regulatory mechanisms and research progress of the NLRP3 inflammasome in multiple myeloma,and discusses potential therapeutic strategies for multiple myeloma targeting the NLRP3 inflammasome,aiming to provide a reference for future research and clinical applications.

Hyperuricemia (HUA) is a metabolic disorder resulting from the excessive accumulation of uric acid in the body. Numerous studies have demonstrated that HUA is closely associated with various reproductive disorders, including erectile dysfunction, polycystic ovary syndrome, and endometriosis. This article presents a comprehensive review of research progress on the relationship between HUA and reproductive disorders, both domestically and internationally. Specifically, it focuses on the potential roles of biological mechanisms, such as oxidative stress, inflammatory responses, endothelial dysfunction, and alterations in the gut microbiota, in the development of reproductive dysfunction. This review aims to offer insights into the mechanisms underlying hyperuricemia-induced reproductive disorders, and to inform potential therapeutic strategies.

Articular cartilage is crucial weight-bearing tissue in the human body,and the maintenance of its biomechanical functions relies on the integrity of the structure. However, due to the lack of blood supply,it is inherently limited in its ability to self-repair after injury, which can readily lead to osteoarthritis and cartilage degenerative diseases.In recent years,adipose derived mesenchymal stem cells (ADSCs) have been widely used in regenerative medicine research due to their abundant sources and convenient isolation.Exosomes derived from these cells through paracrine signaling not only inherit the biological characteristics of the parent cells, but also exhibit low immunogenicity, favorable biobarrier permeability, and high stability, making them essential mediators of intercellular signal transduction. Research has demonstrated that the RNA, proteins, and bioactive factors carried by exosomes derived from ADSCs can regulate immune responses, promote chondrocytes cell proliferation, and enhance the metabolism and activity. Meanwhile, they can also upregulate chondrogenic gene expression and inhibit cartilage-degrading genes, thereby improving the extracellular matrix and promoting cartilage repair. As high-quality nanocarriers for drugs, the combination of exosomes with bioengineering can effectively improve the repair efficiency of damaged cartilage. This review summarizes the applications and mechanisms of ADSCs-derived exosomes in cartilage repair and associated diseases, aiming to provide insights for the standardization of exosome-based therapies and the clinical treatment of cartilage injuries.

Tryptophan 2,3-dioxygenase (TDO2) is one of the key enzymes that mediates the catabolism of tryptophan along the kynurenine pathway. Numerous studies have shown that TDO2 is aberrantly overexpressed in a variety of malignant tumor cells, and is closely associated with tumor progression, immune evasion, and immune suppression within the tumor microenvironment. Consequently, TDO2 has become an essential target that has attracted significant attention for tumor immunotherapy. In recent years, TDO2 inhibitors have been proposed to reverse the immunotolerant state of tumors, enhancing immune responses in the host, thus showing potential in cancer therapy. This article provides an overview of the structure and function of TDO2, as well as its role in immunoregulation, with a particular focus on the applications of TDO2 inhibitors in cancer therapy and the latest research advancements.