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<p>Stroke is the second-leading cause of mortality and the principal contributor to long-term disability worldwide. Despite the widespread clinical implementation of secondary prevention protocols, the 90-day stroke recurrence rate remains a significant concern, particularly among patients with atherosclerosis. Mounting evidence implicates inflammatory pathways as central mediators in both atherogenesis and plaque destabilization. It is known that ischemic stroke triggers a substantial release of cell-free DNA (cfDNA) into the systemic circulation. These nucleic acid fragments can subsequently activate endothelial cells, thereby promoting atherosclerosis, and can also activate nucleotide-sensing inflammasomes within vulnerable plaques, thus triggering thrombotic cascades and early recurrent cerebrovascular events. In this review, we comprehensively examine the pathophysiological origins of cfDNA, delineate its mechanistic involvement in stroke recidivism, and evaluate current therapeutic strategies targeting cfDNA catabolism in the management of ischemic stroke, aiming to provide insights for future research in this field.</p> Graphical abstract <p></p>

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Circulating cfdna: A novel biomarker for preventing early recurrence in ischemic stroke

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月16日

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  • Xinglan Li,
  • Yongjin Yuan,
  • Weiyao Jing,
  • Cui Liu,
  • Mai Wei,
  • Qianru Liu,
  • Xing Li,
  • Long Wei,
  • Xiaozheng Du,
  • Jinhai Wang

摘要

Stroke is the second-leading cause of mortality and the principal contributor to long-term disability worldwide. Despite the widespread clinical implementation of secondary prevention protocols, the 90-day stroke recurrence rate remains a significant concern, particularly among patients with atherosclerosis. Mounting evidence implicates inflammatory pathways as central mediators in both atherogenesis and plaque destabilization. It is known that ischemic stroke triggers a substantial release of cell-free DNA (cfDNA) into the systemic circulation. These nucleic acid fragments can subsequently activate endothelial cells, thereby promoting atherosclerosis, and can also activate nucleotide-sensing inflammasomes within vulnerable plaques, thus triggering thrombotic cascades and early recurrent cerebrovascular events. In this review, we comprehensively examine the pathophysiological origins of cfDNA, delineate its mechanistic involvement in stroke recidivism, and evaluate current therapeutic strategies targeting cfDNA catabolism in the management of ischemic stroke, aiming to provide insights for future research in this field.

Graphical abstract