Erratum to “Effect of Thymoquinone on Acute Kidney Injury Induced by Sepsis in BALB/c Mice”

Guo, Lipeng; Liu, Si-Xu; Yang, Qin; Li, Hongyang; Xu, Lulu; Hao, Yuhua; Zhang, Xiaoqing

doi:10.1155/2020/3182919

Cited by 3 publications

(2 citation statements)

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“…For example, apoptosis and necrosis are found in renal tissue in SA-AKI ( 11 ). Guo et al ( 115 ) and Liu et al ( 116 ) found that apoptosis and pyroptosis coexist in CLP mice. Li and Liu confirmed the same results ( 117 , 118 ).…”

Section: Relationship Between Various Types Programmed Cell Deathmentioning

confidence: 99%

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Deng

Zhou

et al. 2022

Front. Med.

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Sepsis-associated acute kidney injury (SA-AKI) is common in patients with severe sepsis, and has a high incidence rate and high mortality rate in ICU patients. Most patients progress to AKI before drug treatment is initiated. Early studies suggest that the main mechanism of SA-AKI is that sepsis leads to vasodilation, hypotension and shock, resulting in insufficient renal blood perfusion, finally leading to renal tubular cell ischemia and necrosis. Research results in recent years have shown that programmed cell death such as apoptosis, necroptosis, pyroptosis and autophagy play important roles. In the early stage of sepsis-related AKI, autophagy bodies form and inhibit various types of programmed cell death. With the progress of disease, programmed cell death begins. Apoptosis promoter represents caspase-8-induced apoptosis and apoptosis effector represents caspase-3-induced apoptosis, however, caspase-11 and caspase-1 regulate gasdermin D-mediated pyroptosis. Caspase-8 and receptor interacting kinase 1 bodies mediate necroptosis. This review focuses on the pathophysiological mechanisms of various programmed cell death in sepsis-related AKI.

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Section: Relationship Between Various Types Programmed Cell Deathmentioning

confidence: 99%

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Deng

Zhou

et al. 2022

Front. Med.

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“…Caspase-11 knockout strains showed reduced abnormalities in renal structure and serum creatinine levels, indicating improved renal function [ 19 ]. Studies have found that oxidative stress and mitochondrial dysfunction also play a role in septic acute kidney injury [ 46 , 47 ]. Li et al [ 47 ] found that heme oxygenase protects mice against these damaging processes.…”

Section: Implications Of Lps Internalization In Sepsismentioning

confidence: 99%

Intracellular and Extracellular Lipopolysaccharide Signaling in Sepsis: Avenues for Novel Therapeutic Strategies

Gabarin¹,

Zimmel³

et al. 2021

J Innate Immun

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Sepsis is defined as organ dysfunction due to a dysregulated systemic host response to infection. During gram-negative bacterial infection and other acute illness such as absorption from the gut infection, lipopolysaccharide (LPS) is a major mediator in sepsis. LPS is able to trigger inflammation through both intracellular and extracellular pathways. Classical interactions between LPS and host cells first involve LPS binding to LPS binding protein (LBP), a carrier. The LPS-LBP complex then binds to a receptor complex including the CD14, MD2, and toll-like receptor 4 (TLR4) proteins, initiating a signal cascade which triggers the secretion of pro-inflammatory cytokines. However, it has been established that LPS is also internalized by macrophages and endothelial cells through TLR4-independent pathways. Once internalized, LPS is able to bind to the cytosolic receptors caspases-4/5 in humans and the homologous caspase-11 in mice. Bound caspases-4/5 oligomerize and trigger the assembly of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome followed by the activation of inflammatory caspase-1 resulting in subsequent release of interleukin-1β. Caspases-4/5 also activate the perforin gasdermin D and purinergic receptor P2X7, inducing cell lysis and pyroptosis. Pyroptosis is a notable source of inflammation and damage to the lung endothelial barrier during sepsis. Thus, inhibition of caspases-4/5/1 or downstream effectors to block intracellular LPS signaling may be a promising therapeutic approach in adjunction with neutralizing extracellular LPS for treatment of sepsis.

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Plants’ bioactive secondary metabolites in the management of sepsis: Recent findings on their mechanism of action

et al. 2022

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Sepsis is a severe inflammatory response to systemic infection and is a threatening cause of death in intensive care units. In recent years, a number of studies have been conducted on the protective effect of natural products against sepsis-induced organ injury. However, a comprehensive review of these studies indicating the mechanisms of action of the bioactive compounds is still lacking. In this context, this review aimed to provide an updated analysis of the mechanism of action of plants’ secondary metabolites in the management of sepsis. Scopus, Science Direct, Google Scholar, and PubMed were searched from inception to July 2022. A variety of secondary metabolites were found to be effective in sepsis management including allicin, aloin, cepharanthine, chrysin, curcumin, cyanidin, gallic acid, gingerol, ginsenoside, glycyrrhizin, hesperidin, kaempferol, narciclasine, naringenin, naringin, piperine, quercetin, resveratrol, rosmarinic acid, shogaol, silymarin, sulforaphane, thymoquinone, umbelliferone, and zingerone. The protective effects exerted by these compounds can be ascribed to their antioxidant properties as well as induction of endogenous antioxidant mechanisms, and also via the downregulation of inflammatory response and reduction of biochemical and inflammatory markers of sepsis. These findings suggest that these secondary metabolites could be of potential therapeutic value in the management of sepsis, but human studies must be performed to provide strength to their potential clinical relevance in sepsis-related morbidity and mortality reduction.

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Erratum to “Effect of Thymoquinone on Acute Kidney Injury Induced by Sepsis in BALB/c Mice”

Cited by 3 publications

References 1 publication

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Programmed Cell Death in Sepsis Associated Acute Kidney Injury

Intracellular and Extracellular Lipopolysaccharide Signaling in Sepsis: Avenues for Novel Therapeutic Strategies

Plants’ bioactive secondary metabolites in the management of sepsis: Recent findings on their mechanism of action

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