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<p>Regulated cell death (RCD) has emerged as a pivotal upstream mediator supported by correlative preclinical and clinical evidence in the pathogenesis of sepsis-induced coagulopathy (SIC), a life-threatening complication strongly linked to increased mortality. RCD-guided phenotyping integrates pyroptosis, NETosis, ferroptosis, necroptosis, and PANoptosis pathways to systematically redefine SIC — from molecular signatures to targeted interventions. This review comprehensively examines how RCD-derived Damage-Associated Molecular Patterns (DAMPs) mediate coagulation dysfunction, explores subtype-specific biomarkers for patient stratification, and outlines phenotype-directed combination therapies. We further investigate unresolved challenges and future developments in RCD-guided precision immunomodulation, emphasizing the transformative potential of RCD-based frameworks to advance the clinical management of SIC by bridging insights from cell death and thrombosis research.</p> Graphical Abstract <p>Regulated Cell Death-induced Coagulation Dysfunction in Sepsis</p> <p>This graphical abstract summarizes the core framework of the review.</p> <p>(1) Clinical Issues: Sepsis progresses to sepsis-induced coagulopathy (SIC) and disseminated intra-vascular coagulation (DIC), with conventional single-target therapies showing limited efficacy.</p> <p>(2) Core Mechanism: Regulated cell death (RCD) activation triggers the release of damage-associated molecular patterns (DAMPs), which drive coagulation dysfunction.</p> <p>(3) Subtyping &amp; Therapy Module: Based on distinct molecular signatures, SIC can be stratified into four RCD-dominant phenotypes, enabling phenotype-directed targeted therapy.</p> <p>(4) Translational Challenges: Clinical translation is hindered by three key obstacles: unvalidated bi-omarkers, undefined therapeutic time windows, and potential off-target effects of systemic interventions.</p> <p></p>

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Regulated cell death-induced coagulation dysfunction in sepsis

  • 期刊论文

  • 发表日期：

    2026年7月28日

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  • Min Li,
  • Ao Li,
  • Sipin Tan

摘要

Regulated cell death (RCD) has emerged as a pivotal upstream mediator supported by correlative preclinical and clinical evidence in the pathogenesis of sepsis-induced coagulopathy (SIC), a life-threatening complication strongly linked to increased mortality. RCD-guided phenotyping integrates pyroptosis, NETosis, ferroptosis, necroptosis, and PANoptosis pathways to systematically redefine SIC — from molecular signatures to targeted interventions. This review comprehensively examines how RCD-derived Damage-Associated Molecular Patterns (DAMPs) mediate coagulation dysfunction, explores subtype-specific biomarkers for patient stratification, and outlines phenotype-directed combination therapies. We further investigate unresolved challenges and future developments in RCD-guided precision immunomodulation, emphasizing the transformative potential of RCD-based frameworks to advance the clinical management of SIC by bridging insights from cell death and thrombosis research.

Graphical Abstract

Regulated Cell Death-induced Coagulation Dysfunction in Sepsis

This graphical abstract summarizes the core framework of the review.

(1) Clinical Issues: Sepsis progresses to sepsis-induced coagulopathy (SIC) and disseminated intra-vascular coagulation (DIC), with conventional single-target therapies showing limited efficacy.

(2) Core Mechanism: Regulated cell death (RCD) activation triggers the release of damage-associated molecular patterns (DAMPs), which drive coagulation dysfunction.

(3) Subtyping & Therapy Module: Based on distinct molecular signatures, SIC can be stratified into four RCD-dominant phenotypes, enabling phenotype-directed targeted therapy.

(4) Translational Challenges: Clinical translation is hindered by three key obstacles: unvalidated bi-omarkers, undefined therapeutic time windows, and potential off-target effects of systemic interventions.