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Peer-reviewedCC BY 4.0Frontiers in Cell and Developmental Biology

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

  • Lin Lu1,2
  • Hui Lin1,2
  • Peng Zhang3
  • Yun Li1,2
  • Jie Zhang3
  1. 1Department of Medical Research Center, Shaoxing People’s Hospital, Shaoxing, China
  2. 2School of Medicine, Shaoxing University, Shaoxing, China
  3. 3Department of Cardiology, Shaoxing People’s Hospital, Shaoxing, China
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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.

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Cite

BibTeXRIS
BibTeX
@article{lu2026evidencetoclaim,
  title = {{An evidence-to-claim framework for cGAS–STING and AIM2 in atherosclerosis}},
  author = {Lin Lu and Hui Lin and Peng Zhang and Yun Li and Jie Zhang},
  journal = {Frontiers in Cell and Developmental Biology},
  year = {2026},
  month = oct,
  doi = {10.3389/fcell.2026.1999070},
  url = {https://doi.org/10.3389/fcell.2026.1999070},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - An evidence-to-claim framework for cGAS–STING and AIM2 in atherosclerosis
AU  - Lin Lu
AU  - Hui Lin
AU  - Peng Zhang
AU  - Yun Li
AU  - Jie Zhang
PY  - 2026
DA  - 2026/10/22
JO  - Frontiers in Cell and Developmental Biology
DO  - 10.3389/fcell.2026.1999070
UR  - https://doi.org/10.3389/fcell.2026.1999070
AB  - 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.
SN  - 2296-634X
ER  -