Purine metabolic adaptation protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.

Q: What is the clinical evidence from this study?

Population: Atherosclerosis. Intervention: Purine-base supplementation. Primary outcome: DNA damage, apoptosis, barrier dysfunction, and atherogenesis.

Qian Ma; Yongfeng Cai; Zhidan Zhang; Dingwei Zhao; Yuan Zhao; Peishan Xu; Tammy Lu; Wendy Zhang; Qiuhua Yang; Yaqi Zhou; Varadarajan Sudhahar; Tohru Fukai; Hanjoong Jo; Yiming Xu; Yuqing Huo

doi:10.1073/pnas.2526299123

May 5, 2026

Purine metabolic adaptation protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.

View at Publisher

Ask AI

Bookmark

Share

Key result

Purine-base supplementation protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.

Key Points

Investigate how purine metabolism protects endothelial cells from DNA damage and atherosclerosis.
Deleted specific genes to assess their impact on DNA damage and atherogenesis.
Applied purine-base supplementation to evaluate repair capabilities.
Identified MYC as a regulator in the d-flow-MYC-ATIC-DNPS axis.
Deletion leads to increased DNA damage and accelerated atherosclerosis.
Purine-base supplementation significantly improves DNA repair mechanisms.
MYC drives the induction of ATIC, which supports nucleotide sufficiency.

Structured PICO

P

Population

Preclinical model of disturbed flow-induced DNA damage and atherosclerosis

I

Intervention

Purine-base supplementation and genetic deletion (specific gene not stated in abstract fragment)

O

Outcome

DNA damage, apoptosis, endothelial barrier dysfunction, and atherogenesissurrogate

Ask about this paper

Answers are grounded in this paper and cite their sources.

Implication

The study identifies a d-flow-MYC-ATIC-DNPS axis that sustains nucleotide sufficiency for DNA repair, suggesting potential endothelial-targeted therapeutic strategies for atherosclerosis.

Abstract

deletion exacerbates DNA damage, apoptosis, barrier dysfunction, and accelerates atherogenesis, while purine-base supplementation rescues repair defects. We further identify MYC as a mechanosensitive driver of ATIC induction. These findings establish a d-flow-MYC-ATIC-DNPS axis that sustains nucleotide sufficiency for DNA repair and maintains endothelial barrier integrity, suggesting potential endothelial-targeted therapeutic strategies for atherosclerosis.

Discussion

No takes yet. Share an insight, caveat, or question.

Cite This Study

Ma et al. (2026) studied Atherosclerosis. Purine-base supplementation was evaluated on DNA damage, apoptosis, barrier dysfunction, and atherogenesis. Purine-base supplementation rescues repair defects and protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.

synapsesocial.com/papers/69f6e6648071d4f1bdfc70fe https://doi.org/10.1073/pnas.2526299123

View at Publisher

Ask AI

Bookmark

Share

Purine metabolic adaptation protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.

Key Points

Structured PICO

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Purine metabolic adaptation protects the endothelium from disturbed flow-induced DNA damage and atherosclerosis.

Key Points

Structured PICO

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Keep reading

Keep reading