Inflammation: Mechanisms and Disease Links

Inflammation is a coordinated biological response to pathogens, tissue damage, or environmental stressors, involving immune and non-immune cells, signaling pathways, and soluble mediators to restore homeostasis. Acute inflammation is protective, marked by rapid innate immune activation, leukocyte recruitment, and cytokine release (TNF- , IL-1beta, IL-6), with NF- B, MAPK, and JAK/STAT pathways driving gene transcription. Resolution occurs via pro-resolving lipid mediators, anti-inflammatory cytokines, and clearance of apoptotic cells. Dysregulation leads to chronic inflammation, driving autoimmune diseases, cardiovascular disorders, metabolic syndromes, cancers, and neurodegeneration. In CVD, vascular inflammation induces endothelial dysfunction and atherosclerosis; in metabolic disease, low-grade inflammation promotes insulin resistance and NAFLD; in cancer, it fosters genomic instability and immune evasion. Neuroinflammation, mediated by microglia and astrocytes, contributes to Alzheimer's, Parkinson's, and multiple sclerosis. Understanding these mechanisms enables targeted therapies that suppress pathological inflammation while preserving protective functions.

Autorentext
Mona Anwar Mohamed El-Bana, a professor at the National Research Centre, advances medical biochemistry through research and teaching. Her work focuses on disease mechanisms, metabolic disorders, and neurodegeneration. She mentors students, contributes to scientific knowledge, and bridges research with clinical applications for improved healthcare.