Abstract Background Autoimmune diseases (AIDs) refer to a pathological condition in which the body’s immune tolerance mechanism is disrupted or fails to function properly, leading to damage or dysfunction of its own tissues. Most AIDs are chronic and recurrent, severely affecting patients’ quality of life and ability to work. Currently, there is no curative treatment for AIDs; conventional strategies mainly focus on suppressing immune responses and managing symptoms. However, long-term use of these approaches often leads to significant adverse reactions, and some patients respond poorly to therapy. Therefore, new, safe, and effective treatments are urgently needed. Cell therapy, which involves collecting cells via conventional or bioengineering methods, expanding or modifying them in vitro under specific conditions, and then reinfusing them into the body, has emerged as a promising treatment approach. Methods This review summarizes current cell-based therapeutic strategies, their clinical applications, and the key challenges in the context of AIDs. Results Recent studies have reported remarkable outcomes with cell therapy across various diseases, making it a major research focus. Notably, cell therapy offers distinct advantages for treating AIDs, including targeted immune regulation and the potential for durable remission. Nevertheless, it also faces challenges such as complex manufacturing processes, high costs, safety concerns, and variable efficacy. Conclusion Cell therapy is a promising treatment approach for AIDs. However, further research is needed to overcome its current limitations and establish its safety and efficacy in clinical practice.
Abstract Background Acute respiratory distress syndrome (ARDS) is a severe inflammatory lung injury caused by various factors, including infection, trauma and shock. The predominant pathological alteration in its late stages is pulmonary fibrosis (PF), characterised by progressive extracellular matrix deposition, architectural destruction and functional impairment. Particularly in COVID-19-induced ARDS, PF incidence has markedly increased, making it a major sequela impacting patients’ long-term quality of life. Methods This review systematically examines post-acute lung injury (ALI)/ARDS PF through three perspectives: pathogenesis, prediction and treatment. Results Mechanistically, the fibrotic process involves epithelial injury and mesenchymal transition, fibroblast activation with aberrant extracellular matrix remodelling, dysregulated inflammation with immune cell involvement and clinical management-related factors. For prediction, various biomarkers (including growth factors, matrix proteins and inflammatory markers) and imaging features (particularly high-resolution computed tomography (HRCT) and magnetic resonance imaging (MRI) characteristics) demonstrate clinical value. Integrated multiparameter models incorporating artificial intelligence show promise for early identification and risk stratification of high-risk patients. Therapeutic strategies encompass anti-inflammatory approaches (e.g., corticosteroids and antioxidants), antifibrotic agents (pirfenidone and nintedanib), cell-based therapies (mesenchymal stem cells and exosomes) and emerging genetic/RNA interventions. However, specific preventive and therapeutic approaches tailored to the post-ALI/ARDS PF population remain inadequate in clinical practice. Conclusions Future research should focus on elucidating underlying mechanisms, refining early-warning systems, exploring personalised treatments and facilitating clinical translation. The ultimate goal is to transition from traditional supportive care to proactive prevention through enhanced clinical surveillance, early prediction and rational intervention, thereby preventing fibrosis progression and improving outcomes in ARDS survivors.
Abstract Background Prader-Willi syndrome (PWS) is a leading genetic cause of life-threatening obesity, presenting with hypotonia and feeding difficulties in infancy, progressing to hyperphagia, cognitive impairment and behavioural challenges from childhood. It is a rare imprinting disorder caused by gene silencing at the 15q11–q13 locus. Early detection through newborn bloodspot screening (NBS) could enable timely interventions such as growth hormone therapy, dietary management and behavioural support to improve health and developmental outcomes for the affected infants. Methods This review applies the Australian Newborn Bloodspot Screening National Policy Framework as a reference to evaluate the suitability of incorporating PWS into NBS programs. The review outlines benefits and challenges in relation to key criteria used by this Framework, including condition severity, early detection benefits and screening test reliability. Results Emerging screening technologies are recognised for their high sensitivity and specificity and could be integrated into existing NBS workflows using dried blood spots. However, several challenges outlined in this review need to be addressed, including the lack of cost-effectiveness data for population-wide PWS screening programs and the absence of a curative treatment for PWS. Conclusion Expanding NBS to include PWS has the potential to improve health and developmental outcomes through earlier diagnosis and timely interventions. Successful implementation will depend on addressing the remaining challenges.
Abstract Background Necrotizing enterocolitis (NEC) is a leading gastrointestinal emergency in preterm infants, characterized by severe epithelial injury, dysregulated inflammation, and defective mucosal repair. Intestinal stem cells (ISCs) at the crypt base are essential for epithelial renewal and barrier restoration after injury. Methods We summarized recent advances in the molecular and cellular mechanisms governing ISC injury and regeneration in NEC, emphasizing canonical repair pathways, niche-derived regulatory circuits, and emerging ISC-targeted therapies. Results NEC disrupts ISC survival, proliferation, and differentiation through aberrant innate immune activation, microbial dysbiosis, and impairment of Wnt, Notch, and epidermal growth factor (EGF) signalling. ISC function is also shaped by interactions with Paneth cells, mesenchymal niche components, immune cells, and microbial metabolites. Disruption of this niche compromises crypt regeneration, perpetuates barrier dysfunction, and amplifies intestinal inflammation. Restoring ISC activity and niche integrity has therefore prompted interest in growth factor supplementation, microbiota modulation, immune-based interventions, and stem cell-oriented approaches. Conclusions ISC-centred regenerative failure provides an integrated framework linking epithelial biology, immunology, and microbiome research in NEC. Restoring ISC function and niche integrity represents a promising therapeutic direction with experimental and translational relevance.
Bone morphogenetic protein 4 (BMP4) is a member of the transforming growth factor β (TGF-β) superfamily. Accumulating evidence indicates that BMP4 is widely expressed in female reproductive tissues, including the ovary and endometrium. Therefore, this review summarizes the roles of BMP4 in regulating the physiological functions of the ovary and endometrium, including folliculogenesis, ovarian steroidogenesis, endometrial decidualization and regulation of maternal-foetal immunity. Notably, increasing studies revealed that BMP4 is also critically involved in obesity. Given the continuously rising prevalence of obesity worldwide, this review further summarizes emerging evidence on the role of BMP4 in adipogenesis, the shift between white adipose tissue (WAT) and brown adipose tissue (BAT) and metabolic dysregulation. To further elucidate the role of BMP4, we also summarize the expression patterns and potential mechanisms in reproductive disorders and obesity. We found that dysregulated BMP4 expression has been reported in polycystic ovary syndrome (PCOS), recurrent spontaneous abortion (RSA) and obesity, suggesting a potential molecular link between obesity and female fertility. Hence, the potential role of BMP4 between obesity and women’s fertility is further discussed and may provide direction for further reproductive-related research. This hypothesis may guide further studies to explore the underlying mechanisms and their translational implications.
