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Basic science and research
Sepsis-induced cardiac dysfunction: a review of pathophysiology
Reverien Habimana, Insu Choi, Hwa Jin Cho, Dowan Kim, Kyoseon Lee, Inseok Jeong
Acute Crit Care. 2020;35(2):57-66.   Published online May 31, 2020
DOI: https://doi.org/10.4266/acc.2020.00248
  • 8,688 View
  • 601 Download
  • 26 Citations
AbstractAbstract PDF
It is well known that cardiac dysfunction in sepsis is associated with significantly increased mortality. The pathophysiology of sepsis-induced cardiac dysfunction can be summarized as involving impaired myocardial circulation, direct myocardial depression, and mitochondrial dysfunction. Impaired blood flow to the myocardium is associated with microvascular dysfunction, impaired endothelium, and ventriculo-arterial uncoupling. The mechanisms behind direct myocardial depression consist of downregulation of β-adrenoceptors and several myocardial suppressants (such as cytokine and nitric oxide). Recent research has highlighted that mitochondrial dysfunction, which results in energy depletion, is a major factor in sepsis-induced cardiac dysfunction. Therefore, the authors summarize the pathophysiological process of cardiac dysfunction in sepsis based on the results of recent studies.

Citations

Citations to this article as recorded by  
  • A case of sepsis‐induced cardiomyopathy successfully treated with venoarterial extracorporeal membrane oxygenation
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  • Therapeutic potentials of stem cell–derived exosomes in cardiovascular diseases
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  • Extracellular Histone-Induced Protein Kinase C Alpha Activation and Troponin Phosphorylation Is a Potential Mechanism of Cardiac Contractility Depression in Sepsis
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  • Expression of Peripheral Blood DCs CD86, CD80, and Th1/Th2 in Sepsis Patients and Their Value on Survival Prediction
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    Wolfgang Vivas, Sebastian Weis
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  • DAMPs Released from Proinflammatory Macrophages Induce Inflammation in Cardiomyocytes via Activation of TLR4 and TNFR
    Carolina Neu, Yvonne Thiele, Fabienne Horr, Christian Beckers, Nadine Frank, Gernot Marx, Lukas Martin, Sandra Kraemer, Elisabeth Zechendorf
    International Journal of Molecular Sciences.2022; 23(24): 15522.     CrossRef
  • Mitochondrial transplantation protects against sepsis-induced myocardial dysfunction by modulating mitochondrial biogenesis and fission/fusion and inflammatory response
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    Molecular Biology Reports.2022;[Epub]     CrossRef
  • Targeting the TXNIP‐NLRP3 interaction with PSSM1443 to suppress inflammation in sepsis‐induced myocardial dysfunction
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    Journal of Cellular Physiology.2021; 236(6): 4625.     CrossRef
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    Frontiers in Medicine.2021;[Epub]     CrossRef
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  • Deep-learning model for screening sepsis using electrocardiography
    Joon-myoung Kwon, Ye Rang Lee, Min-Seung Jung, Yoon-Ji Lee, Yong-Yeon Jo, Da-Young Kang, Soo Youn Lee, Yong-Hyeon Cho, Jae-Hyun Shin, Jang-Hyeon Ban, Kyung-Hee Kim
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  • Levosimendan versus dobutamine for sepsis-induced cardiac dysfunction: a systematic review and meta-analysis
    Dong-Hua Liu, Yi-Le Ning, Yan-Yan Lei, Jing Chen, Yan-Yan Liu, Xin-Feng Lin, Zhong-Qi Yang, Shao-Xiang Xian, Wei-Tao Chen
    Scientific Reports.2021;[Epub]     CrossRef
  • Exosomes Derived from miR-146a-5p-Enriched Mesenchymal Stem Cells Protect the Cardiomyocytes and Myocardial Tissues in the Polymicrobial Sepsis through Regulating MYBL1
    Chun Liu, Jianhua Xue, Bo Xu, Aixian Zhang, Lili Qin, Jiajia Liu, Yang Yang, Antonio C. Campos de Carvalho
    Stem Cells International.2021; 2021: 1.     CrossRef
Review
Basic science and research
Role of Mitochondrial Oxidative Stress in Sepsis
Harsha Nagar, Shuyu Piao, Cuk-Seong Kim
Acute Crit Care. 2018;33(2):65-72.   Published online May 31, 2018
DOI: https://doi.org/10.4266/acc.2018.00157
  • 7,647 View
  • 393 Download
  • 43 Citations
AbstractAbstract PDF
Mitochondria are considered the power house of the cell and are an essential part of the cellular infrastructure, serving as the primary site for adenosine triphosphate production via oxidative phosphorylation. These organelles also release reactive oxygen species (ROS), which are normal byproducts of metabolism at physiological levels; however, overproduction of ROS under pathophysiological conditions is considered part of a disease process, as in sepsis. The inflammatory response inherent in sepsis initiates changes in normal mitochondrial functions that may result in organ damage. There is a complex system of interacting antioxidant defenses that normally function to combat oxidative stress and prevent damage to the mitochondria. It is widely accepted that oxidative stress-mediated injury plays an important role in the development of organ failure; however, conclusive evidence of any beneficial effect of systemic antioxidant supplementation in patients with sepsis and organ dysfunction is lacking. Nevertheless, it has been suggested that antioxidant therapy delivered specifically to the mitochondria may be useful.

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