Intracerebral hemorrhage (ICH), a common neurological disorder with a high rate of disability, involves complex immunoinflammatory mechanisms, particularly those related to secondary inflammatory injury. Neutrophils, as the earliest subtype of leukocytes recruited after stroke, play a pivotal role in secondary brain injury. Traditionally, neutrophils were thought to mediate tissue damage primarily via phagocytosis, chemotaxis, and degranulation. However, recent studies have shown that neutrophils also contribute to the pathogenesis of intracerebral hemorrhage by releasing neutrophil extracellular traps (NETs), which exacerbate blood-brain barrier disruption, amplify local inflammy -30ation, and promote neuronal injury. This review systematically examines the interactions between the central and peripheral immune systems following ICH. It focuses on the bidirectional regulatory relationship between microglia and neutrophils, and their coordinated roles in inflammation, blood-brain barrier disruption, neurological dysfunction, and cognitive impairment. In addition, this review summarizes recent potential therapeutic strategies targeting the formation and clearance of NETs, including peptidylarginine deiminase 4 inhibitors, reactive oxygen species inhibitors, histone inhibitors, and DNases. These interventions may offer theoretical insights into novel therapeutic targets for mitigating secondary injury following ICH.

Mesenchymal stem cells (MSCs) have demonstrated distinct advantages in skeletal muscle repair owing to their self-renewal capacity, multidirectional differentiation potential, and immunomodulatory functions. As a critical regulator of skeletal muscle regeneration, MSCs have been shown to ameliorate skeletal muscle injury induced by factors such as wasting and metabolic disorders through the activation of satellite cell function, inhibition of myofiber atrophy, and regulation of protein metabolic balance. In the treatment of myasthenia gravis (MG), the therapeutic effects of MSCs are exerted through dual mechanisms: first, autoantibody production is reduced via immunomodulation, thereby alleviating immune-mediated attacks at neuromuscular junctions; second, secondary muscle atrophy is delayed by preserving the integrity of neuromuscular signaling. Notably, MSC function is closely associated with acetylcholine metabolism, neuromuscular junction stability, and the aging microenvironment, in which aging-induced MSC decline may exacerbate intramuscular fat infiltration and impair regenerative capacity. In this paper, the biological properties of mesenchymal stem cells (MSCs) and their regulatory roles in skeletal muscle metabolic and injury-related abnormalities are systematically reviewed, and the fundamental significance of MSCs in skeletal muscle repair and myasthenia gravis (MG) therapy is elucidated through multiple mechanisms, including immunomodulation, neuroprotection, and muscle fiber regeneration. Furthermore, the bottlenecks of clinical translation (including cell source selection, phenotypic stability, and efficacy heterogeneity) are analyzed, and the challenges and optimization strategies for clinical application are discussed, with the aim of providing theoretical references for regenerative medicine research in neuromuscular diseases. However, clinical translation studies have indicated that the actual efficacy of most MSC-based therapies is considerably lower than that observed in in vitro experiments. This discrepancy may be attributed to low post-transplantation cell survival, inadequate homing efficiency, and the adverse influence of a senescent microenvironment that impairs cellular function. It has been indicated by recent studies that strategies, including optimization of cell sources and preparation protocols (e.g., the use of allogeneic MSCs derived from adipose tissue or umbilical cord with standardized production), incorporation of biomaterial supports (such as hydrogel-based encapsulation), and adoption of combination therapies (e.g., co-administration with neurotrophic factors or targeted drugs), can effectively improve the delivery efficiency and therapeutic outcomes of MSCs.

Vascular calcification (VC) is a critical pathological condition associated with significant morbidity and mortality. This study employs a hybrid approach of network pharmacology and molecular biology to delineate the therapeutic mechanisms of salidroside (SAL), an active compound from Rhodiola crenulata, against VC. Through database mining and network analysis, 388 SAL targets intersecting with 2871 VC-associated targets were identified, resulting in 208 common targets. A protein-protein interaction (PPI) network constructed via the String database and topological analysis in Cytoscape 3.9.1 pinpointed 10 key targets, including IL6, TNF, TP53, IL1B, HIF1A, CASP3, and STAT3, among others. The identified genes were concentrated in the lipid and atherosclerosis pathways, indicating that the improvement of VC by SAL may occur through the regulation of abnormal expression of lipid and inflammatory factors. It was also found that SAL inhibits the abnormal expression of inflammatory factors, thereby activating the JAK2/STAT3 pathway to intervene in the progression of VC. The JAK2/STAT3 pathway is a key molecular mechanism by which SAL prevents further deterioration of VC. Functional enrichment analyses revealed the involvement of these targets in inflammatory responses and lipid metabolism, pivotal pathways in VC. In vivo studies in rats demonstrated SAL's efficacy in mitigating dyslipidemia and vascular inflammation, with improved serum lipid profiles and reduced vascular calcium deposition. The mechanistic exploration, grounded in Western blot analysis, demonstrated salidroside's ability to regulate the JAK2/STAT3 signaling pathway, highlighting its potential as a modulator in this critical molecular mechanism and offering a potential therapeutic target for VC. The strength of this research lies in its methodological rigor, integrating computational predictions with in vivo validations. This comprehensive approach establishes a robust framework for exploring the therapeutic mechanisms of natural compounds in combating VC.

Cardiovascular diseases (CVDs) are among the main factors impacting negatively human health on a global scale. Every year, there is an increase in the prevalence of CVDs despite advancements in therapy for managing traditional risk factors. Research on exosomes is has garnered great interest due to their role in regulating intercellular communication. Exosome‑mediated epigenetic regulation is involved in the interaction between circulating cells and blood arteries, as well as in intercellular communication processes, and exosomes serve as biomarkers of cell activation. The present study aimed to summarize the recent research on exosome‑mediated epigenetic regulation mechanisms, as well as the roles of exosomes in the pathology and diagnosis of CVDs, which may increase the current understanding of the precise functions that exosomes play in the development of CVDs.

Vascular calcification (VC) is a critical pathological condition associated with significant morbidity and mortality. This study employs a hybrid approach of network pharmacology and molecular biology to delineate the therapeutic mechanisms of salidroside (SAL), an active compound from Rhodiola crenulata, against VC. Through database mining and network analysis, 388 SAL targets intersecting with 2871 VC-associated targets were identified, resulting in 208 common targets. A protein-protein interaction (PPI) network constructed via the String database and topological analysis in Cytoscape 3.9.1 pinpointed 10 key targets, including IL6, TNF, TP53, IL1B, HIF1A, CASP3, and STAT3, among others. The identified genes were concentrated in the lipid and atherosclerosis pathways, indicating that the improvement of VC by SAL may occur through the regulation of abnormal expression of lipid and inflammatory factors. It was also found that SAL inhibits the abnormal expression of inflammatory factors, thereby activating the JAK2/STAT3 pathway to intervene in the progression of VC. The JAK2/STAT3 pathway is a key molecular mechanism by which SAL prevents further deterioration of VC. Functional enrichment analyses revealed the involvement of these targets in inflammatory responses and lipid metabolism, pivotal pathways in VC. In vivo studies in rats demonstrated SAL's efficacy in mitigating dyslipidemia and vascular inflammation, with improved serum lipid profiles and reduced vascular calcium deposition. The mechanistic exploration, grounded in Western blot analysis, demonstrated salidroside's ability to regulate the JAK2/STAT3 signaling pathway, highlighting its potential as a modulator in this critical molecular mechanism and offering a potential therapeutic target for VC. The strength of this research lies in its methodological rigor, integrating computational predictions with in vivo validations. This comprehensive approach establishes a robust framework for exploring the therapeutic mechanisms of natural compounds in combating VC.