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Peer-reviewedCC BY 4.0Frontiers in Immunology

NF-κB signaling as a central integrator of inflammation, stress-induced metabolic dysfunction, and cardiomyocyte fate in sepsis-induced myocardial injury

  • Haitang Liao1
  • Yuling Zhou1
  • Xiangwen Weng1
  • Dongsheng Ren1
  • Wenhui Guo1
  • Chenyang Duan1,2,3
  • Ming Wang4
  • Zhenchun Luo1
4 affiliations
  1. 1Department of Critical and Emergency Medicine, Chongqing Hospital of Traditional Chinese Medicine
  2. 2Department of Anesthesiology, The Second Affiliated Hospital of Chongqing Medical University
  3. 3Basic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, Ministry of Education, The Second Affiliated Hospital of Chongqing Medical University
  4. 4Department of Cardiology, Chongqing Hospital of Traditional Chinese Medicine
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Abstract

Sepsis-induced myocardial injury is a frequent and life-threatening complication of sepsis, characterized by transient yet profound cardiac dysfunction that markedly worsens patient outcomes. Despite extensive investigation, the molecular mechanisms linking systemic inflammation to myocardial metabolic failure and cardiomyocyte loss remain incompletely understood. Emerging evidence indicates that nuclear factor-κB (NF-κB) signaling functions as more than a canonical inflammatory pathway in this context. In this review, we propose a unifying framework in which NF-κB serves as a central integrator linking inflammatory stress, stress-induced metabolic dysfunction, and cardiomyocyte fate in sepsis-induced myocardial injury. We summarize how NF-κB-driven inflammatory amplification, through crosstalk with MAPK signaling and immune cell activation, reshapes the myocardial immune microenvironment. We further discuss how NF-κB interfaces with oxidative stress, mitochondrial dysfunction, redox imbalance, and ferroptosis-related metabolic stress, thereby disrupting cardiomyocyte homeostasis. Importantly, NF-κB is highlighted as a context-dependent determinant of cardiomyocyte fate, modulating apoptosis, pyroptosis, and non-apoptotic cell death programs under septic conditions. Finally, we discuss emerging NF-κB-directed therapies and the need for tissue-specific combination strategies. This integrative framework may guide more precise therapeutic development for sepsis-induced myocardial injury.

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Cite

BibTeXRIS
BibTeX
@article{liao2026nfκb,
  title = {{NF-κB signaling as a central integrator of inflammation, stress-induced metabolic dysfunction, and cardiomyocyte fate in sepsis-induced myocardial injury}},
  author = {Haitang Liao and Yuling Zhou and Xiangwen Weng and Dongsheng Ren and Wenhui Guo and Chenyang Duan and Ming Wang and Zhenchun Luo},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1807015},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1807015/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - NF-κB signaling as a central integrator of inflammation, stress-induced metabolic dysfunction, and cardiomyocyte fate in sepsis-induced myocardial injury
AU  - Haitang Liao
AU  - Yuling Zhou
AU  - Xiangwen Weng
AU  - Dongsheng Ren
AU  - Wenhui Guo
AU  - Chenyang Duan
AU  - Ming Wang
AU  - Zhenchun Luo
PY  - 2026
DA  - 2026/10/20
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1807015
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1807015/full
AB  - Sepsis-induced myocardial injury is a frequent and life-threatening complication of sepsis, characterized by transient yet profound cardiac dysfunction that markedly worsens patient outcomes. Despite extensive investigation, the molecular mechanisms linking systemic inflammation to myocardial metabolic failure and cardiomyocyte loss remain incompletely understood. Emerging evidence indicates that nuclear factor-κB (NF-κB) signaling functions as more than a canonical inflammatory pathway in this context. In this review, we propose a unifying framework in which NF-κB serves as a central integrator linking inflammatory stress, stress-induced metabolic dysfunction, and cardiomyocyte fate in sepsis-induced myocardial injury. We summarize how NF-κB-driven inflammatory amplification, through crosstalk with MAPK signaling and immune cell activation, reshapes the myocardial immune microenvironment. We further discuss how NF-κB interfaces with oxidative stress, mitochondrial dysfunction, redox imbalance, and ferroptosis-related metabolic stress, thereby disrupting cardiomyocyte homeostasis. Importantly, NF-κB is highlighted as a context-dependent determinant of cardiomyocyte fate, modulating apoptosis, pyroptosis, and non-apoptotic cell death programs under septic conditions. Finally, we discuss emerging NF-κB-directed therapies and the need for tissue-specific combination strategies. This integrative framework may guide more precise therapeutic development for sepsis-induced myocardial injury.
SN  - 1664-3224
ER  -