Exosome‐mediated pyroptosis of miR‐93‐TXNIP‐NLRP3 leads to functional difference between M1 and M2 macrophages in sepsis‐induced acute kidney injury

Juan, Chenxia; Mao, Yan Ping; Cao, Qian; Yan, Chen; Zhou, Li-Na; Sheng, Li; Chen, Hao; Chen, Jia He; Zhou, Guo Ping; Jin, Rui

doi:10.1111/jcmm.16449

Cited by 76 publications

(43 citation statements)

References 46 publications

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“…Both M1 and M2 macrophages participate in the process of AKI by influencing the levels of inflammatory factors and cell death, including pyroptosis. Juan et al ( 95 ) proved that M1 and M2 macrophages have opposite effects on the pyroptosis of renal TECs in a co-culture system, which may lead to functional differences of their different phenotypes in the pathology of sepsis-AKI. Additional evidence showed that either CLP or LPS caused macrophage pyroptosis ( 93 , 96 ).…”

Section: Types Of Programmed Cell Death In Sepsis-akimentioning

confidence: 99%

The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

Wang

et al. 2021

Front. Med.

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Sepsis is a systemic inflammatory response syndrome caused by infection, following with acute injury to multiple organs. Sepsis-induced acute kidney injury (AKI) is currently recognized as one of the most severe complications related to sepsis. The pathophysiology of sepsis-AKI involves multiple cell types, including macrophages, vascular endothelial cells (ECs) and renal tubular epithelial cells (TECs), etc. More significantly, programmed cell death including apoptosis, necroptosis and pyroptosis could be triggered by sepsis in these types of cells, which enhances AKI progress. Moreover, the cross-talk and connections between these cells and cell death are critical for better understanding the pathophysiological basis of sepsis-AKI. Mitochondria dysfunction and oxidative stress are traditionally considered as the leading triggers of programmed cell death. Recent findings also highlight that autophagy, mitochondria quality control and epigenetic modification, which interact with programmed cell death, participate in the damage process in sepsis-AKI. The insightful understanding of the programmed cell death in sepsis-AKI could facilitate the development of effective treatment, as well as preventive methods.

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Section: Types Of Programmed Cell Death In Sepsis-akimentioning

confidence: 99%

The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

Wang

et al. 2021

Front. Med.

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“…The regulation of macrophage activation has been under extensive investigation, particularly at the transcriptional and epigenetic levels ( 8 , 27 , 28 ). The latest research has shown that miRNAs are involved in a variety of pathogeneses by regulating macrophage activation ( 29 ). However, although a much larger number of lncRNAs is found in mammalian cells, the role of regulating macrophage activation remains poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Tanreqing Injection Attenuates Macrophage Activation and the Inflammatory Response via the lncRNA-SNHG1/HMGB1 Axis in Lipopolysaccharide-Induced Acute Lung Injury

Tan

et al. 2022

Front. Immunol.

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The etiology of acute lung injury (ALI) is not clear, and the treatment of ALI presents a great challenge. This study aimed to investigate the pathogenesis and potential therapeutic targets of ALI and to define the target gene of Tanreqing (TRQ), which is a traditional Chinese medicine formula composed of five medicines, scutellaria baicalensis, bear bile powder, goat horn powder, honeysuckle and forsythia. Macrophage activation plays a critical role in many pathophysiological processes, such as inflammation. Although the regulation of macrophage activation has been extensively investigated, there is little knowledge of the role of long noncoding RNAs (lncRNAs) in this process. In this study, we found that lncRNA-SNHG1 expression is distinctly regulated in differently activated macrophages in that it is upregulated in LPS. LncRNA-SNHG1 knockdown attenuates LPS-induced M1 macrophage activation. The SNHG1 promoter was bound by NF-κB subunit p65, indicative of SNHG1 being a direct transcriptional target of LPS-induced NF-κB activation. SNHG1 acts as a proinflammatory driver that leads to the production of inflammatory cytokines and the activation of macrophages and cytokine storms by physically interacting with high-mobility group box 1 (HMGB1) in ALI. TRQ inhibited NF-κB signaling activation and binding of NF-κB to the SNHG1 promoter. In conclusion, this study defined TRQ target genes, which can be further elucidated as mechanism(s) of TRQ action, and provides insight into the molecular pathogenesis of ALI. The lncRNA-SNHG1/HMGB1 axis is an ideal therapeutic for ALI treatment.

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“…Chen et al isolated exosomes from M1 and M2 macrophages, and miRNA sequencing revealed differential miRNA expression levels in M1 and M2 exosomes, in which miR-93-5p was involved in the regulation of mouse renal tubular epithelial cells pyroptosis. It was determined that thioredoxin-interacting protein (TXNIP) was a direct target of miR-93-5p in mouse renal tubular epithelial cells ( 77 ).…”

Section: Immune Cells Promote Various Types Of Programmed Cell Deaths...mentioning

confidence: 99%

Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury

Deng

et al. 2022

Front. Med.

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A growing number of studies have confirmed that immune cells play various key roles in the pathophysiology of acute kidney injury (AKI) development. After the resident immune cells and intrinsic renal cells are damaged by ischemia and hypoxia, drugs and toxins, more immune cells will be recruited to infiltrate through the release of chemokines, while the intrinsic cells promote macrophage polarity conversion, and the immune cells will promote various programmed deaths, phenotypic conversion and cycle arrest of the intrinsic cells, ultimately leading to renal impairment and fibrosis. In the complex and dynamic immune microenvironment of AKI, the bidirectional interaction between immune cells and intrinsic renal cells affects the prognosis of the kidney and the progression of fibrosis, and determines the ultimate fate of the kidney.

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Exosome‐mediated pyroptosis of miR‐93‐TXNIP‐NLRP3 leads to functional difference between M1 and M2 macrophages in sepsis‐induced acute kidney injury

Cited by 76 publications

References 46 publications

The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI

Tanreqing Injection Attenuates Macrophage Activation and the Inflammatory Response via the lncRNA-SNHG1/HMGB1 Axis in Lipopolysaccharide-Induced Acute Lung Injury

Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury

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