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Cardiomyocyte death in sepsis: Mechanisms and regulation (Review)
Geping Zhang1, Dan Dong1, Xianyao Wan1
1Department of Critical Care Medicine, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116011, P.R. China.
Insights
Sepsis can cause heart dysfunction by damaging heart cells. Understanding how these cells die through various pathways is crucial for developing new treatments for sepsis-induced cardiac dysfunction.
Area of Science:
- Cardiology
- Molecular Biology
- Immunology
Background:
- Sepsis-induced cardiac dysfunction is a common and complex complication of sepsis.
- Cardiomyocyte loss significantly impairs cardiac function due to limited regenerative capacity.
- Inflammatory pathways critically influence cardiomyocyte function and death in sepsis.
Purpose of the Study:
- To review current understanding of cardiomyocyte death pathways in sepsis.
- To explore the role of inflammatory activation in regulating these death mechanisms.
- To identify therapeutic targets for sepsis-induced cardiac dysfunction.
Main Methods:
- Literature review of sepsis-induced cardiomyocyte death pathways.
- Analysis of inflammatory signaling and cardiomyocyte death modes.
- Examination of cross-regulation between different cell death mechanisms.
Main Results:
- Sepsis activates multiple cardiomyocyte death pathways, including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy.
- Inflammatory signaling diversely regulates these death mechanisms.
- Cross-regulation between death modes impacts overall cardiac function in sepsis.
Conclusions:
- Understanding sepsis-induced cardiomyocyte death pathways is vital for therapeutic development.
- Targeting specific signaling pathways and their cross-regulation offers potential treatment strategies.
- Further research into these mechanisms can provide a basis for treating sepsis-induced cardiac dysfunction.
Abstract:
Sepsis‑induced cardiac dysfunction is one of the most common types of organ dysfunction in sepsis; its pathogenesis is highly complex and not yet fully understood. Cardiomyocytes serve a key role in the pathophysiology of cardiac function; due to the limited ability of cardiomyocytes to regenerate, their loss contributes to decreased cardiac function. The activation of inflammatory signalling pathways affects cardiomyocyte function and modes of cardiomyocyte death in sepsis. Prevention of cardiomyocyte death is an important therapeutic strategy for sepsis‑induced cardiac dysfunction. Thus, understanding the signalling pathways that activate cardiomyocyte death and cross‑regulation between death modes are key to finding therapeutic targets. The present review focused on advances in understanding of sepsis‑induced cardiomyocyte death pathways, including apoptosis, necroptosis, mitochondria‑mediated necrosis, pyroptosis, ferroptosis and autophagy. The present review summarizes the effect of inflammatory activation on cardiomyocyte death mechanisms, the diversity of regulatory mechanisms and cross‑regulation between death modes and the effect on cardiac function in sepsis to provide a theoretical basis for treatment of sepsis‑induced cardiac dysfunction.
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