Endothelial–Immune Crosstalk in Vascular Inflammation: Molecular Circuits of Injury, Repair, and Remodeling

Vascular inflammatory disorders arise from dynamic and reciprocal interactions between endothelial cells and immune populations that reshape vessel function and structure. Endothelial activation alters barrier integrity, coagulation, and adhesion molecule expression, enabling leukocyte recruitment and amplification of inflammatory cues within the vascular wall. In turn, immune-derived mediators such as cytokines, TNF-family ligands, complement, and alarmins reprogram endothelial signaling and transcriptional states, promoting tissue injury and dysregulated repair. Recent advances in single-cell and spatial profiling, proteomics, and systems immunology have revealed substantial heterogeneity across endothelial and immune subsets, vascular beds, and disease stages. However, the mechanistic “switches” that translate these molecular programs into functional vascular outcomes remain incompletely defined.This Research Topic aims to showcase mechanistic and causality-oriented studies that dissect endothelial–immune crosstalk across contexts of vascular inflammation and remodeling. We seek contributions that identify pathway-level circuits governing endothelial activation, immune recruitment, vascular permeability, cell death/survival, and structural remodeling, and that link these circuits to measurable vascular phenotypes. We particularly welcome work integrating patient-relevant evidence with rigorous experimental validation, for example via genetic or pharmacologic perturbations, organoid or vascular-on-chip systems, and in vivo models. By bridging vascular biology, immunology, and quantitative approaches, this collection will clarify how inflammatory signaling networks are initiated, sustained, and resolved, and will illuminate actionable nodes for therapeutic intervention and biomarker development.We welcome Original Research, Reviews, Mini-Reviews, Methods, and Perspectives addressing: (i) endothelial barrier dysfunction, glycocalyx injury, and thrombo-inflammation; (ii) adhesion/chemokine axes controlling leukocyte recruitment and retention; (iii) cytokine/TNF-family, interferon, IL-1/IL-6, and complement signaling in vascular inflammation; (iv) transcriptional and epigenetic regulators (e.g., NF-κB, AP-1, STATs) and post-translational control (ubiquitin–proteostasis) shaping endothelial responses; (v) immune–stromal–endothelial interactions driving intimal hyperplasia, aneurysm formation, and fibrosis; and (vi) multi-omics, spatial, and interpretable computational analyses supported by functional validation. Purely correlative studies without mechanistic or phenotypic linkage are discouraged. Topic editors: Hongbiao Huang, Xuan Li, Sara Sabbagh Source: https://www.frontiersin.org/research-topics/78381/endothelial-immune-crosstalk-in-vascular-inflammation-molecular-circuits-of-injury-repair-and-remodeling