Small airway disease (SAD) is a pathological condition that affects the bronchioles and non-cartilaginous airways 2 mm or less in diameter. These airways play a crucial role in respiratory function and are often implicated in various pulmonary disorders. Pulmonary fibrotic diseases are characterized by the thickening and scarring of lung tissue, leading to progressive respiratory failure. We aimed to present the link between SAD and fibrotic lung conditions. The evidence suggests that SAD may act as a precursor or exacerbating factor in the progression of fibrotic diseases. Patients with fibrotic conditions often exhibit signs of small airway dysfunction, which can contribute to worsening respiratory symptoms and decreased lung function. Moreover, individuals with advanced SAD are at a heightened risk of developing fibrotic changes in the lung. The interplay between inflammation, environmental factors, and genetic predisposition further complicates this association. The early detection and management of SAD can potentially mitigate the progression of fibrotic diseases, highlighting the need for comprehensive clinical evaluation and research. This review emphasizes the need to understand the evolving connection between SAD and pulmonary fibrosis, urging further detailed research to clarify the causes and potential treatment between the two entities.

The biological functions of osteopontin (OPN) are diverse and specific to physiological and pathophysiological conditions implicated in inflammation, biomineralization, cardiovascular diseases, cellular viability, cancer, diabetes, and renal stone disease. We aimed to present the role of OPN in respiratory health and disease. OPN influences the immune system and is a chemo-attractive protein correlated with respiratory disease severity. There is evidence that OPN can advance the disease stage associated with its fibrotic, inflammatory, and immune functions. OPN contributes to eosinophilic airway inflammation. OPN can destroy the lung parenchyma through its neutrophil influx and fibrotic mechanisms, linking OPN to at least one of the two major chronic obstructive pulmonary disease phenotypes. Respiratory diseases that involve irreversible lung scarring, such as idiopathic pulmonary disease, are linked to OPN, with protein levels being overexpressed in individuals with severe or advanced stages of the disorders and considerably lower levels in those with less severe symptoms. OPN plays a significant role in lung cancer progression and metastasis. It is also implicated in the pathogenesis of pulmonary hypertension, coronavirus disease 2019, and granuloma generation.

Sepsis remains a leading global cause of mortality, with delayed recognition and empirical antibiotic overuse fueling poor outcomes and rising antimicrobial resistance. This systematic scoping review evaluates the current landscape of artificial intelligence (AI) and machine learning (ML) applications in sepsis care, focusing on early detection, personalized antibiotic management, and resistance forecasting. Literature from 2019 to 2025 was systematically reviewed following PRISMA-ScR guidelines. A total of 129 full-text articles were analyzed, with study quality assessed via the JBI and QUADAS-2 tools. AI-based models demonstrated robust predictive performance for early sepsis detection (AUROC 0.68–0.99), antibiotic stewardship, and resistance prediction. Notable tools, such as InSight and KI.SEP, leveraged multimodal clinical and biomarker data to provide actionable, real-time support and facilitate timely interventions. AI-driven platforms showed potential to reduce inappropriate antibiotic use and nephrotoxicity while optimizing outcomes. However, most models are limited by single-center data, variable interpretability, and insufficient real-world validation. Key challenges remain regarding data integration, algorithmic bias, and ethical implementation. Future research should prioritize multicenter validation, seamless integration with clinical workflows, and robust ethical frameworks to ensure safe, equitable, and effective adoption. AI and ML hold significant promise to transform sepsis management, but their clinical impact depends on transparent, validated, and user-centered deployment.

Recent studies indicate a significant relationship between malnutrition, frailty, and pleural effusion (PE), highlighting the critical role of muscle mass in patient outcomes. This review investigates the association between sarcopenia—characterized by a decline in skeletal muscle mass and function—and PE, marked by fluid accumulation in the pleural space. The findings reveal that sarcopenia is prevalent in patients with PE and is linked to increased postoperative complications and mortality rates. In liver transplantation, esophagectomy, and lung cancer surgeries, sarcopenia exacerbates the risk of adverse outcomes. Notably, preoperative muscle mass assessment serves as a predictive tool for identifying patients at higher risk of complications. This review underscores the importance of early diagnosis and intervention for sarcopenia to improve clinical outcomes in PE patients. The therapeutic approach should include comprehensive nutritional evaluations and targeted muscle-strengthening interventions. By addressing sarcopenia, healthcare providers can significantly reduce PE-related complications, enhance patient recovery, and improve survival rates. This review provides a foundation for future research to develop effective strategies for the management and treatment of sarcopenia in the context of PEs, aiming to optimize patient care and quality of life.

Skeletal muscle dysfunction and exercise intolerance are major extrapulmonary manifestations of chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), yet their severity is not fully predicted by pulmonary impairment. This narrative review examines extracellular vesicles (EVs) as candidate mediators of lung–muscle communication within a broader network of inflammatory, metabolic, vascular, nutritional, and inactivity-related mechanisms. The evidence is asymmetrical. COPD provides direct human skeletal muscle evidence for quadriceps microRNA dysregulation, impaired protein synthesis and mitochondrial function, oxidative stress, and abnormalities of the regenerative microvascular niche; however, none of these observations demonstrates delivery of pathogenic cargo from the lung by EVs. In IPF, EV-mediated epithelial–mesenchymal signalling, fibroblast activation, and profibrotic remodelling are well supported within the lung, whereas skeletal muscle effects remain indirect. Accordingly, the lung–muscle EV axis should be viewed as a biologically plausible, evidence-weighted hypothesis rather than an established causal pathway. Progress will require experiments that identify the cellular source of EVs, trace their vascular transit and skeletal muscle uptake, and demonstrate functional cargo transfer using EV-depletion, rescue, and integrated muscle readouts. Conventional size and morphology measurements do not reliably distinguish muscle- from lung-derived EVs; source discrimination currently depends more on molecular cargo and cell-associated markers. Hypoxia and transient or sustained oxygen desaturation may modify EV release and cargo through HIF- and redox-sensitive signalling, but disease-specific evidence connecting these changes to lung-to-muscle transfer in COPD or IPF remains limited.