Work

An evidence-to-claim framework for cGAS–STING and AIM2 in atherosclerosis

Year: 2026
Type: review
Abstract: Cytosolic self-DNA sensing has been implicated in atherosclerosis, but similar pathway readouts are often interpreted as equivalent across cell compartments and disease stages. We evaluate DNA identity and localization, node causality, cellular lineage, and endpoint relevance before assigning a biological or therapeutic inference. Within the evidence considered in this focused narrative review, the STING signaling adaptor is most directly linked to disturbed-flow-associated endothelial dysfunction. In macrophage and hematopoietic compartments, STING-node dependence supports chronic inflammatory amplification. Vascular smooth muscle cell studies support a DNA-damage-associated STING-node stress program, whereas the requirement for cell-autonomous cGAS signaling and structural causality remains unresolved. AIM2 is a parallel, context- and stage-dependent axis in JAK2V617F clonal hematopoiesis, selected advanced-plaque models, and acute post-stroke neutrophil extracellular trap (NET)-DNA exposure. These settings map to distinct endpoints and should not be treated as interchangeable therapeutic indications. This focused narrative review applies an author-developed heuristic framework rather than a validated evidence-grading instrument; none of the studies considered fulfilled the complete same-model L2/N2/C2/E2 benchmark.
Language: English
Subfield: Immunology
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W7223182506
FWCI:
Cites: 76
Cited by:
Related to: 10