Beyond canonical inflammatory signaling: emerging mechanisms in autoinflammation and immune dysregulation

Inflammation is a highly coordinated response essential for host defense and tissue homeostasis. However, persistent or dysregulated inflammatory signaling can drive chronic tissue damage and contribute to a broad spectrum of immune-mediated, autoinflammatory, metabolic, and cardiovascular diseases. Increasing evidence indicates that inflammatory responses are regulated by complex and interconnected molecular mechanisms that extend beyond canonical signaling pathways.This Research Topic aims to highlight emerging mechanisms regulating inflammatory signaling and their contribution to disease pathogenesis. We particularly welcome studies investigating the molecular and cellular regulation of NF-κB and other transcriptional pathways, innate immune sensing, inflammasome activation, cytokine and chemokine signaling, cellular stress responses, immunometabolism, epigenetic regulation, and alternative splicing and isoform-specific functions. Contributions addressing the interplay between inflammatory signaling and vascular, cardiovascular, metabolic, or tissue-specific dysfunction are also encouraged.A particular focus will be placed on how alterations in inflammatory signaling contribute to autoinflammatory and immune dysregulation, including in rare and metabolic disorders such as Fabry disease. Studies identifying novel molecular mechanisms, disease-associated inflammatory signatures, biomarkers, or therapeutic targets are highly encouraged.We welcome contributions covering, but not limited to, the following themes:- Molecular and transcriptional regulation on autoinflammation: Novel mechanisms controlling NF-κB, alternative transcriptional cascades, and isoform-specific functions via alternative splicing.- Innate immune sensing and effector signaling: Signaling networks governing pattern recognition receptors, inflammasome activation, and cytokine/chemokine cascades.- Immunometabolism and cellular stress: mitochondrial homeostasis and endoplasmic reticulum (ER) stress responses driving or sustaining inflammation- Epigenetic and post-transcriptional control: Chromatin remodeling, histone modifications, DNA methylation, and non-coding RNA regulation of inflammatory genes.- Inflammatory signaling in rare disorders: Mechanisms underlying tissue-specific, vascular, cardiovascular, and autoinflammatory manifestations, including rare metabolic disorders (e.g., Fabry disease). We welcome Original Research, Reviews, Mini Reviews, Perspectives, and other relevant article types addressing these topics from molecular, cellular, translational, and clinical perspectives.By bringing together complementary perspectives across inflammation, innate immunity, vascular biology, rare diseases, and molecular signaling, this Research Topic aims to advance our understanding of emerging mechanisms underlying dysregulated inflammation and to foster the development of more precise diagnostic and therapeutic strategies. Topic editors: Johannes A. Schmid, Giuseppa Biddeci, Francesco Di Blasi Source: https://www.frontiersin.org/research-topics/86170/beyond-canonical-inflammatory-signaling-emerging-mechanisms-in-autoinflammation-and-immune-dysregulation