Lysosomal storage disorders (LSD) are a rare class of diseases caused by mutations in genes encoding lysosomal hydrolases, leading to metabolic disorders. These disorders arise from either the absence of functional lysosomal hydrolases or damage to the lysosomes. Impaired degradation of complex macromolecules leads to the accumulation of substrates in tissues and subsequent dysfunction of cells and organs. Current treatment options for LSDs primarily include enzyme replacement therapy, substrate reduction therapy, and chaperone therapy. However, most of these treatments do not cure the disease, but merely delay its progression. They necessitate continuous administration of medications, which can be financially burdensome, and often fail to effectively reach target sites due to various challenges, resulting in diminished therapeutic effects. Therefore, there is an urgent need for more effective and thorough treatment options. Extracellular vesicles (EVs) are naturally secreted components with potential applications in various diseases. However, their role and therapeutic potential in the context of LSDs remain unclear. This article summarizes current research progress on EVs in two common LSDs, Fabry disease and Gaucher disease, by reviewing literature from PubMed. It discusses biomarkers associated with EVs in the diagnosis and treatment of LSDs, as well as advancements in engineered EVs for therapeutic applications.

Treatment-resistant depression (TRD) is a severe mental illness that poses a significant threat to the health and well-being of patients. In recent years, TRD has garnered increased attention from scholars both domestically and internationally. Currently, there is ongoing debate regarding the definition of TRD. Clinical treatment strategies for TRD primarily include optimizing drug dosage and duration, switching medications, combining drugs, and employing synergistic therapies. Additionally, various animal models of TRD, based on different pathological changes, have been successfully established and utilized in research to reveal the potential pathogenesis of TRD, such as excessive inflammatory responses, hyperactivity of the hypothalamic-pituitary-adrenal axis, dysregulation of the glutamatergic system, and disturbances in tryptophan metabolism. These findings have generated new insights for the development of novel medications for TRD, with some candidates currently in the pipeline having achieved significant breakthroughs. This review comprehensively discusses these issues, aiming to provide a reference for future research and drug development in TRD.

Despite remarkable advances in drug therapy for chronic heart failure (CHF), the related morbidity, mortality and hospitalizations remain substantial. Novel device-based interventions have emerged as potential therapies for CHF. Recently, interatrial shunt device (IASD), baroreflex activation therapy (BAT), and phrenic nerve stimulation (PNS) have shown promise in treating patients with CHF. This article summarizes the working principles and clinical research outcomes of these innovative therapeutic devices, and analyzes their advantages and disadvantages, potential risks, and future application prospects, aiming to provide new insights and references for clinical treatment.

Multilineage differentiating stress enduring (Muse) cells are a newly discovered type of stem cells that have attracted increasing attention due to their superior abilities compared to mesenchymal stem cells, such as enhanced tri-germ layer differentiation potential, stress tolerance, homing ability, in situ differentiation capacity, and non-tumorigenicity. Muse cells have shown promising effects in various animal disease models and clinical trials, highlighting their immense potential for applications in the field of regenerative medicine. However, the extremely low baseline levels of Muse cells in vivo pose a challenge for conventional culture methods, which often fail to obtain large quantities of high-purity Muse cells within a short time frame, limiting their translational applications. This article aims to discuss the characteristics and culture methods of Muse cells, as well as research progress in disease models and specific clinical trials, providing a theoretical basis for further studies on Muse cells.

Cardiovascular diseases significantly affect human health and represent an urgent public health issue that needs to be addressed.Reactive oxygen species (ROS) generated by mitochondrial metabolism are risk factors for the occurrence and progression of cardiovascular diseases. When mitochondrial function is impaired,excess ROS are generated.If the endogenous antioxidant system fails to eliminate the excess ROS,oxidative stress damage occurs,thereby compromising cardiovascular health.Therefore,improving mitochondrial function and reducing ROS through nutritional interventions has become a crucial approach to prevent and treat cardiovascular diseases.Mitoquinol mesylate (MitoQ),a mitochondria-targeted antioxidant,accumulates in the inner mitochondrial membrane,quenching mitochondrial ROS.This article reviews the molecular properties and mechanisms of action of MitoQ,as well as its benefits in improving cardiovascular diseases.Additionally,it compares the similarities and differences between MitoQ and coenzyme Q10 (CoQ10),providing a scientific basis for the future application of MitoQ in the treatment of cardiovascular diseases.

MG53(mitsugumin 53) is a member of the tripartite motif (TRIM) protein family of E3 ubiquitin ligases,also known as TRIM72.MG53 is a cell membrane repair protein widely expressed in cardiac and skeletal muscles,capable of rapidly accumulating at the site of membrane injury, playing a crucial role in the repair of cardiac and skeletal muscle cell membranes. In recent years, numerous studies have found that MG53 participates in the myocardial protective effect of ischemic preconditioning and postconditioning, and mitigates myocardial ischemia-reperfusion injury. Moreover, it is expressed in various organs, promoting cell membrane repair under physiological or pathological conditions. However, MG53 overexpression leads to decreased expression of the ubiquitin-dependent insulin receptor, contributing to metabolic syndrome and diabetic heart disease. This article reviews the recent advances in the physiological functions and associated mechanisms of MG53 protein, aiming to provide a reference for the clinical application of recombinant human mitsugumin53 (rhMG53).

Exosomes are extracellular vesicles secreted by cells into the extracellular space, carrying abundant biomolecules such as proteins, nucleic acids and metabolites. MicroRNAs(miRNAs) are non-coding RNA molecules that play important roles in cell differentiation, proliferation, and survival.Exercise can induce the secretion of exosomes,and promote the biological effects of the contained miRNAs.Recent studies have indicated a close relationship between exosomal miRNAs and chronic heart failure,exercise can alter the expression of exosomal miRNAs in body fluids and tissues.Exosomal miRNAs serve as biomarkers for the diagnosis and prognosis of heart failure,potentially ameliorating heart failure by inhibiting myocardial fibrosis,promoting myocardial mitochondrial function,and enhancing myocardial cell survival. Therefore,this article reviews the role of exosomal miRNAs in chronic heart failure and the mitochondrial mechanisms through which exercise improves chronic heart failure via exosomal miRNAs, offering a valuable basis for future diagnosis and treatment of heart failure.

The significance of redox homeostasis in the functional adaptation, injury repair, and health maintenance of skeletal muscle has been increasingly recognized. Redox homeostasis in skeletal muscle is a dynamic equilibrium process that precisely regulates the generation and clearance of reactive oxygen species (ROS). This regulation enables skeletal muscle to effectively cope with oxidative stress induced by exercise, thereby promoting cellular health and functional recovery. Moderate ROS generation helps activate the antioxidant system and facilitates adaptive responses in muscle. As crucial signaling molecules, ROS play significant roles in skeletal muscle metabolism, antioxidant responses, mitochondrial function, and protein synthesis during exercise. However, excessive ROS can trigger oxidative stress, damaging the structure and function of muscle cells, leading to muscle degeneration. This review comprehensively explores the regulatory mechanisms of redox homeostasis in skeletal muscle, particularly the processes of ROS generation and clearance. It also examines the impact of exercise on the redox status of skeletal muscle, with a focus on analyzing signaling pathways related to oxidative stress, especially the roles of the Nrf2/KEAP1 and HSP72/HSF1 pathways during exercise. In-depth research into redox signaling pathways and their regulatory mechanisms under different exercise modalities is crucial for optimizing exercise training programs, improving skeletal muscle health, and preventing and treating associated diseases.

Hyperuricemia(HUA) is a pathological condition characterized by elevated levels of uric acid in the blood,which can adversely affect female reproductive health by altering the functions of the uterus and ovaries.Epigenetic modifications, primarily influenced by environmental factors,regulate gene expression without changing the gene sequence,thereby affecting individual metabolism,and being transmitted to the offspring through epigenetic imprinting. The occurrence of HUA results from the interaction between genetic and environmental factors. Understanding the underlying epigenetic mechanisms is of great significance for effective prevention and treatment of HUA and its complications. This article discusses in detail the effects of maternal HUA on pregnancy complications,gestational metabolic syndrome,and offspring health. It summarizes the epigenetic regulatory mechanisms of HUA, aiming to elucidate the pathogenesis of HUA at the molecular level and provide new research insights for reducing maternal pregnancy risks.

The liver plays a crucial role in the transformation and clearance of xenobiotics.However, continuous exposure to high concentrations of these foreign substances can lead to liver damage,known as drug-induced liver injury (DILI).The pregnane X receptor (PXR), a member of the nuclear receptor superfamily,is a key regulator of hepatic drug clearance.PXR regulates the expression of drug-metabolizing enzymes and transporters,and plays an essential role in drug transformation, metabolism, and clearance in the liver. Studies have shown that PXR mediates the occurrence and progression of DILI. This article aims to briefly review the role and mechanisms of PXR in DILI.

Periodontitis is a common oral disease and the leading cause of tooth loss in adults. The gingival epithelium is the first line of defense against external invasions. The occurrence and development of periodontitis are closely related to the invasion and destruction of the gingival epithelium by various pathogenic bacteria. Research has demonstrated that periodontitis-associated pathogens destroy the gingival epithelium,invade deep tissues,and trigger inflammatory responses through a series of virulence factors. Among them, Porphyromonas gingivalis is the main cause of periodontitis. This article reviews the regulatory effects of Porphyromonas gingivalis on the gingival epithelium, with the aim of providing a reference for the treatment of periodontitis.

High-temperature requirement factor A3 (HtrA3) is a serine protease, which has been identified as an important target molecule in diseases such as cancer and pregnancy complications. The regulatory role of this molecule is attributed to its extensive biological functions. However, there is still a lack of effective integration regarding this aspect. Therefore, in this article, we discuss the biological functions of HtrA3,including its involvement in protein quality control, immune regulation,maintenance of mitochondrial homeostasis,apoptosis,extracellular matrix degradation, and epithelial-mesenchymal transformation, as well as its role in regulating cell proliferation and migration. In addition, studies have confirmed that HtrA3 is predominantly expressed in the heart, with significant research progress made regarding this molecule in the contexts of myocardial fibrosis, heart failure, and ischemia-reperfusion injury. Given its extensive functions, HtrA3 may serve as a significant regulator of cardiovascular diseases, highlighting its important research value in the development of cardiovascular diseases.