Osteoarthritis (OA) is a prevalent degenerative joint disorder characterized by progressive cartilage destruction, chronic inflammation, pain, and functional impairment. Conventional therapies primarily focus on symptom management and are unable to restore damaged articular cartilage or effectively modify disease progression. Consequently, increasing attention has been directed toward biologic and regenerative approaches that target the underlying mechanisms of cartilage degeneration and joint dysfunction. This review provides a comprehensive overview of emerging regenerative strategies for articular cartilage repair, including gene- and noncoding RNA-based therapies, platelet-rich plasma (PRP), bone marrow aspirate concentrate (BMAC), mesenchymal stromal cells (MSCs), MSC-derived exosomes, and cell-based interventions. Current evidence indicates that these therapies exert their effects through modulation of inflammatory pathways, enhancement of extracellular matrix synthesis, promotion of chondrocyte survival, and regulation of tissue repair processes. Among them, PRP and BMAC offer minimally invasive approaches with favorable safety profiles, whereas MSCs and exosome-based therapies demonstrate substantial regenerative and immunomodulatory potential. Gene and epigenetic therapies further provide opportunities to target disease-associated molecular pathways and improve cartilage homeostasis. Despite encouraging preclinical and clinical outcomes, significant challenges remain, including heterogeneity in biologic preparations, variability in treatment protocols, limited long-term clinical evidence, and the absence of standardized outcome measures. Future research should focus on mechanistic validation, protocol standardization, optimization of delivery strategies, and large-scale randomized clinical trials to establish the long-term safety and disease-modifying efficacy of these regenerative therapies. Collectively, biologic and regenerative interventions represent promising avenues for advancing cartilage repair and improving clinical outcomes in patients with osteoarthritis.
Haiyuan Yue, Ahmad Alhaskawi, S. Ezzi et al.· Frontiers in Pharmacology· 0 citations
Pulmonary macrophages are essential regulators of immune surveillance, tissue homeostasis, and inflammatory responses within the respiratory microenvironment. Emerging evidence indicates that chronic environmental stress and persistent injury induce profound immunometabolic remodeling in these cells, thereby contributing to the development and progression of chronic lung diseases. Under physiological conditions, pulmonary macrophages maintain metabolic homeostasis primarily through oxidative phosphorylation and fatty acid oxidation. However, pathological conditions drive metabolic reprogramming characterized by altered glycolysis, mitochondrial dysfunction, oxidative stress, lipid dysregulation, and disturbed iron homeostasis, leading to persistent inflammation, impaired tissue repair, and progressive remodeling. Recent studies have further highlighted the critical interplay between metabolic pathways, redox signaling, and immune regulation in shaping macrophage phenotypes and functions. Importantly, therapeutic strategies targeting macrophage metabolism and redox balance, together with advances in macrophage-directed drug delivery systems, have emerged as promising approaches for modulating pulmonary inflammation and tissue injury. This review summarizes recent understanding of immunometabolic remodeling in pulmonary macrophages under homeostatic and pathological conditions and discusses emerging therapeutic perspectives targeting macrophage metabolism in chronic respiratory diseases.
Zhen Yuan, Ahmad Alhaskawi, Yejiang Tang et al.· Frontiers in Pharmacology· 0 citations