Innate immune signaling and inflammatory amplification in inflammation-driven diseases: mechanisms, biomarkers, and therapeutic targeting

Inflammation immunology has emerged as a central field for understanding the balance between host defense and pathological immune activation. Inflammation-driven diseases often result from excessive activation of innate immune sensing pathways that trigger uncontrolled cytokine cascades and cell death mechanisms. This escalating immune response can lead to tissue damage, failure of resolution pathways, and chronic remodeling. Recent research has shed light on key players in inflammatory amplification, including inflammasomes, the cGAS-STING pathway, macrophage and neutrophil inflammatory programs, oxidative stress, ferroptosis, and metabolic reprogramming. Despite these advances, major gaps remain in deciphering how acute innate immune overactivation transitions into chronic inflammation and therapeutic refractoriness. There is a pressing need to integrate new molecular insights with translational approaches that can identify reliable biomarkers and guide targeted interventions to restore immune balance.This Research Topic aims to elucidate the cellular and molecular foundations of inflammatory storm responses within the framework of innate immune regulation. It seeks to advance understanding of how innate immune signaling triggers pathological amplification loops leading to tissue injury and chronic immune dysregulation. The goal is to define mechanisms that connect immune sensing to inflammatory amplification, determine the role of cell-type-specific effector programs, and identify biomarkers with mechanistic and diagnostic value. Additionally, this topic aims to explore and evaluate therapeutic strategies designed to modulate innate immune activation and attenuate inflammation-driven tissue damage, fostering translational insight into targeted anti-inflammatory therapy development.To gather further insights into inflammation-driven immunopathology, this Research Topic is limited to mechanistically oriented investigations directly linking innate immunity with inflammatory amplification. Submissions that are purely descriptive or lack mechanistic depth are outside the scope. We welcome articles addressing, but not limited to, the following themes:• Cytokine storm signaling and inflammatory amplification• Innate immune sensing pathways, including inflammasome and cGAS-STING signaling• Macrophage, monocyte, and neutrophil programs in inflammatory tissue injury• Oxidative stress, ferroptosis, and metabolic rewiring in inflammation-driven damage• Resolution failure, chronic inflammatory remodeling, and immune dysregulation• Inflammation-associated therapeutic refractoriness to immune-targeted therapies• Mechanism-based biomarkers of inflammatory activity, tissue injury, and treatment response• Targeted anti-inflammatory and immune-modulating therapeutic strategiesWe welcome original research articles, reviews, systematic reviews, methods papers, and translational studies that focus on mechanistic understanding, biomarker development, or therapeutic targeting of inflammatory amplification processes. Topic editors: Zhirui Zeng, Xinpei Deng, Divya Gopinath Source: https://www.frontiersin.org/research-topics/83165/innate-immune-signaling-and-inflammatory-amplification-in-inflammation-driven-diseases-mechanisms-biomarkers-and-therapeutic-targeting