Inflammatory and cell-survival signaling pathways

Inflammatory and cell-survival signaling pathways encompass a broad array of interconnected molecular circuits, including the NF-κB, PI3K/Akt/mTOR, MAPK/ERK, and JAK/STAT pathways, which coordinate cellular responses to stress and external signals (PMID: 29942082). These pathways are essential for normal physiological processes such as the innate immune response and tissue repair, but their chronic activation is a hallmark of many pathological states (PMID: 30214692). In cancer, dysregulated survival signaling allows malignant cells to evade apoptosis and resist chemotherapy, while in autoimmune diseases, overactive inflammatory pathways lead to tissue destruction (PMID: 28848419). Pharmacological modulation of these pathways aims to selectively inhibit overactive nodes to reduce inflammation or induce apoptosis in diseased cells. However, because these pathways are central to many homeostatic functions, therapeutic targeting requires a careful balance to avoid significant systemic toxicity and to overcome compensatory mechanisms that often lead to treatment resistance (PMID: 31064752).

Other names

Pro-inflammatory signaling cascadesCell survival networksInflammatory signaling pathwaysSurvival signaling pathwaysInflammation and survival signaling

Drugs targeting these pathways typically act as inhibitors of specific signaling nodes, such as cytokine receptors, protein kinases (e.g., JAK, PI3K, MAPK), or anti-apoptotic proteins, thereby blocking the transmission of signals that promote inflammation and cell longevity (PMID: 31064752).