Sepsis‐Induced Cardiomyopathy: Oxidative Implications in the Initiation and Resolution of the Damage

Tsolaki, Vasiliki; Makris, Demosthènes; Mantzarlis, Konstantinos; Zakynthinos, Epameinontas

doi:10.1155/2017/7393525

Cited by 58 publications

(50 citation statements)

References 136 publications

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“…15) TNFα was shown to cause a dose-dependent decrease in LVEF in a septic shock model. 18) IL-1 cooperated with TNFα to enhance the decrease in myocardial contractility. 17) IL-6 exerted negative inotropic effects on sepsis-induced cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

CTRP12 Ameliorated Lipopolysaccharide-Induced Cardiomyocyte Injury

Zhou

Jin

et al. 2020

CHEMICAL & PHARMACEUTICAL BULLETIN

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C1q/tumor necrosis factor (TNF)-related protein 12 (CTRP12) is a secretory protein that participates in the regulation of glucose and lipid metabolism in obesity and diabetes. Its role in cardiovascular disease, particularly sepsis-induced cardiac injury, is unclear. Here, we stimulated cardiomyocytes with lipopolysaccharide (LPS) to establish an in vitro cardiomyocyte injury model and CTRP12 was overexpressed with an adenovirus delivery system. Overexpression of CTRP12 reduced the transcription and release of pro-inflammatory cytokines from LPS-stimulated cardiomyocytes, including TNFα, interleukin-1 (IL-1), and IL-6. Reactive oxygen species (ROS) level increased and the oxidation/redox system was disturbed in LPS-stimulated cardiomyocytes, as evident from the decrease in superoxide dismutase activity and an increase in reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and malondialdehyde level. CTRP12 overexpression decreased the increasing level of ROS and ameliorated the unbalance in the oxidation/redox system in LPS-stimulated cardiomyocytes. The viability of cardiomyocytes decreased after LPS stimulation, and the cells underwent apoptosis. CTRP12-overexpressing cardiomyocytes showed a decrease in the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)positive cells, and the ratio of B cell lymphoma (Bcl)-1/Bax in these cells was recovered. In comparison with the control group, LPS-stimulated cardiomyocytes showed reduced expression of nuclear factor E2-related factor 2 (NRF2), while CTRP12-overexpressing cardiomyocytes showed elevated NRF2 expression. Smallinterfering RNA-mediated silencing of NRF2 expression in cardiomyocytes resulted in the inhibition of the protective effects of CTRP12. Thus, CTRP12 ameliorated injury in LPS-stimulated cardiomyocytes in an NRF2-dependent manner.

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Section: Discussionmentioning

confidence: 99%

CTRP12 Ameliorated Lipopolysaccharide-Induced Cardiomyocyte Injury

Zhou

Jin

et al. 2020

CHEMICAL & PHARMACEUTICAL BULLETIN

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“…Generation of reactive oxygen species (ROS) associated with sepsis is known as one of the most deleterious causes of oxidative damage. Three potential sources of ROS have been proposed to be responsible for this release: mitochondrial, xanthine oxidase, and NADPH oxidase [10–12]. In the context of sepsis, ROS generation by the mitochondria further stimulates ROS production in endothelial cells, triggering a vicious cycle of free radical production resulting in a wide variety of reversible and irreversible toxic modifications on biomolecules [12–14].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of UCP2 Expression Protects against LPS-Induced Oxidative Stress and Apoptosis in Cardiomyocytes

Huang

Peng

Zheng

et al. 2019

Oxidative Medicine and Cellular Longevity

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Uncoupling protein 2 (UCP2) has a cardioprotective role under septic conditions, but the underlying mechanism remains unclear. This study aimed at investigating the effects of UCP2 on the oxidative stress and apoptosis of cardiomyocytes induced by lipopolysaccharide (LPS). First, LPS increased UCP2 expression in cardiomyocytes in a time-dependent manner. LPS increased the production of lactate dehydrogenase (LDH), reactive oxygen species (ROS), and malondialdehyde (MDA) and decreased the level of superoxide dismutase (SOD). However, UCP2 knockdown increased the LPS-induced cardiac injury and oxidative stress. In addition, LPS damaged the mitochondrial ultrastructure and led to the disruption of mitochondrial membrane potential (MMP), as well as the release of mitochondrial cytochrome c. UCP2 knockdown aggravated mitochondrial injury and the release of mitochondrial cytochrome c. LPS increased the protein levels of Bax and cleaved-caspase-3, decreased the protein level of Bcl-2, and upregulated the protein level of mitogen-activated protein kinase. However, upon UCP2 knockdown, the protein levels of Bax and cleaved-caspase-3 increased even further, and the protein level of Bcl-2 was further decreased. The protein level of phosphorylated p38 was also further enhanced. Thus, UCP2 protects against LPS-induced oxidative stress and apoptosis in cardiomyocytes.

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“…While there are still some patients with sepsis who have fully adjusted preload and afterload, LVSD still exists, which may be explained by differential of gene expression, metabolic effects and endotoxin-induced structural and functional changes of the heart. [ 4 , 26 ]…”

Section: Left Ventricular Systolic Dysfunction Vs mentioning

confidence: 99%

Induction and deduction in sepsis-induced cardiomyopathy: five typical categories

Wang¹,

Wang²,

Liu³

et al. 2020

Chinese Medical Journal

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Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The heart is one of the most important oxygen delivery organs, and dysfunction significantly increases the mortality of the body. Hence, the heart has been studied in sepsis for over half a century. However, the definition of sepsis-induced cardiomyopathy is not unified yet, and the conventional conception seems outdated: left ventricular systolic dysfunction (LVSD) along with enlargement of the left ventricle, recovering in 7 to 10 days. With the application of echocardiography in intensive care units, not only LVSD but also left ventricular diastolic dysfunction, right ventricular dysfunction, and even diffuse ventricular dysfunction have been seen. The recognition of sepsis-induced cardiomyopathy is gradually becoming complete, although our understanding of it is not deep, which has made the diagnosis and treatment stagnate. In this review, we summarize the research on sepsis-induced cardiomyopathy. Women and young people with septic cardiomyopathy are more likely to have LVSD, which may have the same mechanism as stress cardiomyopathy. Elderly people with ischemic cardiomyopathy and hypertension tend to have left ventricular diastolic dysfunction. Patients with mechanical ventilation, acute respiratory distress syndrome or other complications of increased right ventricular afterload mostly have right ventricular dysfunction. Diffuse cardiac dysfunction has also been shown in some studies; patients with mixed or co-existing cardiac dysfunction are more common, theoretically. Thus, understanding the pathophysiology of sepsis-induced cardiomyopathy from the perspective of critical care echocardiography is essential.

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Sepsis‐Induced Cardiomyopathy: Oxidative Implications in the Initiation and Resolution of the Damage

Cited by 58 publications

References 136 publications

CTRP12 Ameliorated Lipopolysaccharide-Induced Cardiomyocyte Injury

CTRP12 Ameliorated Lipopolysaccharide-Induced Cardiomyocyte Injury

Upregulation of UCP2 Expression Protects against LPS-Induced Oxidative Stress and Apoptosis in Cardiomyocytes

Induction and deduction in sepsis-induced cardiomyopathy: five typical categories

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