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<p>Sepsis is a life-threatening syndrome resulting from a dysregulated host immune response to infection and is frequently accompanied by coagulation abnormalities and multiple organ dysfunction. As central regulators at the intersection of hemostasis, inflammation, and immunity, platelets play a critical role in the initiation and progression of sepsis. Beyond their traditional function in hemostasis, platelets actively participate in immune modulation, inflammatory amplification, and immunothrombosis. This review systematically summarizes the molecular and cellular mechanisms through which platelets contribute to organ injury in sepsis, with particular emphasis on platelet–immune cell interactions. We discuss how these processes drive the development of acute lung injury, myocardial depression, hepatic and renal dysfunction, and disseminated intravascular coagulation. In addition, we examine the dynamic alterations in platelet phenotype and function during sepsis and their clinical implications. Ultimately, we evaluate the therapeutic potential of antiplatelet strategies, addressing current challenges and future directions for translating platelet-targeted interventions into effective treatments for sepsis.</p>

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Platelet homeostasis and heterogeneity in inflammation and sepsis: mechanisms, biological effects, and clinical potential

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月16日

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  • Yiyun Pan,
  • Wenling Zhao,
  • Beibei Yu,
  • Ji Zhang,
  • Mengdi Qu,
  • Ruiwen Jiang,
  • Tingye Xu,
  • Dongliang Li,
  • Hao Zhang,
  • Changhong Miao

摘要

Sepsis is a life-threatening syndrome resulting from a dysregulated host immune response to infection and is frequently accompanied by coagulation abnormalities and multiple organ dysfunction. As central regulators at the intersection of hemostasis, inflammation, and immunity, platelets play a critical role in the initiation and progression of sepsis. Beyond their traditional function in hemostasis, platelets actively participate in immune modulation, inflammatory amplification, and immunothrombosis. This review systematically summarizes the molecular and cellular mechanisms through which platelets contribute to organ injury in sepsis, with particular emphasis on platelet–immune cell interactions. We discuss how these processes drive the development of acute lung injury, myocardial depression, hepatic and renal dysfunction, and disseminated intravascular coagulation. In addition, we examine the dynamic alterations in platelet phenotype and function during sepsis and their clinical implications. Ultimately, we evaluate the therapeutic potential of antiplatelet strategies, addressing current challenges and future directions for translating platelet-targeted interventions into effective treatments for sepsis.