MOLECULAR MECHANISMS OF INFLAMMATION IN DISEASE PROGRESSION AND THERAPEUTIC TARGETING

Abstract

Inflammation is a fundamental biological response required for host defense, tissue repair, and maintenance of homeostasis. Although acute inflammation is protective and self-limiting, persistent or dysregulated inflammation contributes to the initiation and progression of many chronic diseases. This review aims to examine the molecular mechanisms through which inflammation influences disease progression and to discuss major therapeutic targets and emerging anti-inflammatory strategies. Inflammatory responses are coordinated by immune and non-immune cells, including macrophages, neutrophils, lymphocytes, endothelial cells, epithelial cells, and stromal cells. These cells communicate through cytokines, chemokines, prostaglandins, reactive oxygen species, and damage-associated molecular patterns. Key signaling pathways, including NF-κB, JAK/STAT, MAPK, Toll-like receptor signaling, and inflammasome activation, regulate inflammatory gene expression, immune-cell recruitment, and tissue remodeling. When inflammation fails to resolve, sustained cytokine production, oxidative stress, immune dysregulation, fibrosis, angiogenesis, and extracellular matrix remodeling promote disease progression in cancer, autoimmune disorders, cardiovascular disease, metabolic dysfunction, neurodegeneration, and chronic infections. Therapeutic targeting of inflammatory pathways has advanced substantially through corticosteroids, non-steroidal anti-inflammatory drugs, biologics, cytokine blockade, JAK inhibitors, COX inhibitors, and emerging inflammasome inhibitors. Understanding the molecular basis of inflammation is essential for developing precise and effective therapies. Future strategies should focus on biomarker-guided treatment, resolution-based therapies, RNA-based approaches, microbiome modulation, and personalized interventions that suppress pathological inflammation while preserving protective immunity.