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Purpose of Review <p>Cardiogenic shock (CS) is one of the leading causes of mortality in patients with acute cardiac disease, and systemic inflammation plays a critical role in its pathophysiology. This review explores the role of interleukin-6 (IL-6) in CS, with a focus on its biological pathways, prognostic value, and potential as a therapeutic target, highlighting the importance of addressing inflammation in this context.</p> Recent Findings <p>Recent evidence highlights systemic inflammation implied in CS progression. Among the various cytokines involved, IL-6 is a major pro-inflammatory cytokine associated with organ dysfunction, and high mortality rates in acute myocardial infarction complicated by CS. Mechanistic studies exhibited an involvement of IL-6 since the first stages of CS onset, suggesting its role as both a biomarker and likely a mediator of CS.</p> Summary <p>IL-6 emerges as a key inflammatory mediator in CS pathophysiology, serving as a prognostic biomarker and a potential therapeutic target. Future research should focus on further understanding the underlying mechanism linking acute inflammation and CS, patient phenotyping, and optimizing anti-inflammatory strategies investigating IL-6-targeted therapies to improve outcomes in this poor prognosis condition. Clinical trials of IL-6 blockade in cardiogenic shock are lacking.</p>

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Interleukin-6 in Cardiogenic Shock

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月30日

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  • Luca Fazzini,
  • Michele Golino,
  • Francesco Moroni,
  • Matteo Castrichini,
  • Gregorio Tersalvi,
  • Paolo Manca,
  • Antonio Abbate

摘要

Purpose of Review

Cardiogenic shock (CS) is one of the leading causes of mortality in patients with acute cardiac disease, and systemic inflammation plays a critical role in its pathophysiology. This review explores the role of interleukin-6 (IL-6) in CS, with a focus on its biological pathways, prognostic value, and potential as a therapeutic target, highlighting the importance of addressing inflammation in this context.

Recent Findings

Recent evidence highlights systemic inflammation implied in CS progression. Among the various cytokines involved, IL-6 is a major pro-inflammatory cytokine associated with organ dysfunction, and high mortality rates in acute myocardial infarction complicated by CS. Mechanistic studies exhibited an involvement of IL-6 since the first stages of CS onset, suggesting its role as both a biomarker and likely a mediator of CS.

Summary

IL-6 emerges as a key inflammatory mediator in CS pathophysiology, serving as a prognostic biomarker and a potential therapeutic target. Future research should focus on further understanding the underlying mechanism linking acute inflammation and CS, patient phenotyping, and optimizing anti-inflammatory strategies investigating IL-6-targeted therapies to improve outcomes in this poor prognosis condition. Clinical trials of IL-6 blockade in cardiogenic shock are lacking.