Necroptosis in pulmonary macrophages promotes silica-induced inflammation and interstitial fibrosis in mice

Tao, Huihui; Ge, Deyong; Liao, Juan; Shao, Luocheng; Mo, Aowei; Hu, Lelin; Xu, Ke; Wu, Jing; Mu, Min; Li, Bin; Tao, Xinrong; Wang, Jianhua

doi:10.1016/j.toxlet.2021.11.015

Cited by 10 publications

(4 citation statements)

References 32 publications

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“…There was strong colocalization between the necroptosis-related markers, p-MLKL, and the markers of macrophages, CD68 and F4/80. In agreement with our results, several recently published studies also demonstrated that macrophage necroptosis was involved as part of the mechanism of enhancing inflammatory responses ( 21 – 23 ).…”

Section: Discussionsupporting

confidence: 93%

Enterococcus faecalis -Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis

Dai

Jiang

et al. 2022

Microbiol Spectr

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Section: Discussionsupporting

confidence: 93%

Enterococcus faecalis -Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis

Dai

Jiang

et al. 2022

Microbiol Spectr

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“…[29] Higher levels of IL-6 have also been reported in a mouse model of silicosis. [30] According to multiple studies, IL-6 has been identified as playing a crucial role in the chronic inflammatory phase of silicosis. Furthermore, both macrophages and fibroblasts are known to produce IL-6, which contributes to the development of lung fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Unraveling the mechanism of tetrandrine combined with Buyang Huanwu Decoction against silicosis using network pharmacology and molecular docking analyses

Zhao

et al. 2023

Medicine

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Silicosis is an incurable chronic disease characterized by lung fibrosis and inflammation. The combination of tetrandrine and Buyang Huanwu Decoction (BYHWD) has a curative effect on silicosis. However, the mechanism of action and the key active constituent in BYHWD are still unclear. The present study employed network pharmacology and molecular docking to determine the mechanism of action and the key active components of BYHWD of Tetrandrine in combination with BYHWD for silicosis. The primary elements and targets of BYHWD were obtained from the Traditional Chinese Medicine Systems Pharmacology and analysis platform. The targets associated with tetrandrine and silicosis were identified and extracted from the Comparative Toxicogenomics Database and GeneCards database. The potential targets for the treatment of silicosis using a combination of Tetrandrine and BYHWD were identified by considering the overlapping targets between compound drugs and silicosis. These targets were then utilized to construct protein-protein interaction networks, compound drug-ingredient-target networks, and perform enrichment analyses. The top 5 active ingredients present in the compound drug-ingredient-target network are tetrandrine, quercetin, luteolin, kaempferol, and beta-carotene. Similarly, the top 6 hub genes in the protein-protein interaction network are FGF2, MMP-9, MMP-1, IL-10, IL-17A, and IL-6. The molecular docking suggested that the active components may easily access the active pocket of the hub gene. The in-silico investigation suggested that quercetin might be the active component in BYHWD responsible for therapeutic effectiveness against silicosis. This study identified the active compound and potential molecular mechanism underlying the therapeutic effects of BYHWD in combination with tetrandrine for treating silicosis. Notably, we found that quercetin may serve as the key compound in BYHWD for the treatment of silicosis.

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“…Necroptosis of pulmonary macrophages exhibits the activation in silicosis lungs 155 . Macrophage necroptosis facilitates silica‐mediated inflammatory response and fibrogenesis 155 . The process can be ameliorated by Nec‐1, providing a possible insight into drug discovery and clinical therapy of silicosis.…”

Section: Implications Of Small Molecular Inhibitors Of Necroptosis In...mentioning

confidence: 99%

“…Silicosis owns the features of massive lung nodules and pulmonary fibrosis. Necroptosis of pulmonary macrophages exhibits the activation in silicosis lungs 155 . Macrophage necroptosis facilitates silica‐mediated inflammatory response and fibrogenesis 155 .…”

Section: Implications Of Small Molecular Inhibitors Of Necroptosis In...mentioning

confidence: 99%

Cell type‐specific molecular mechanisms and implications of necroptosis in inflammatory respiratory diseases

Guo,

Zhou,

Wang

et al. 2023

Immunological Reviews

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SummaryNecroptosis is generally considered as an inflammatory cell death form. The core regulators of necroptotic signaling are receptor‐interacting serine–threonine protein kinases 1 (RIPK1) and RIPK3, and the executioner, mixed lineage kinase domain‐like pseudokinase (MLKL). Evidence demonstrates that necroptosis contributes profoundly to inflammatory respiratory diseases that are common public health problem. Necroptosis occurs in nearly all pulmonary cell types in the settings of inflammatory respiratory diseases. The influence of necroptosis on cells varies depending upon the type of cells, tissues, organs, etc., which is an important factor to consider. Thus, in this review, we briefly summarize the current state of knowledge regarding the biology of necroptosis, and focus on the key molecular mechanisms that define the necroptosis status of specific cell types in inflammatory respiratory diseases. We also discuss the clinical potential of small molecular inhibitors of necroptosis in treating inflammatory respiratory diseases, and describe the pathological processes that engage cross talk between necroptosis and other cell death pathways in the context of respiratory inflammation. The rapid advancement of single‐cell technologies will help understand the key mechanisms underlying cell type‐specific necroptosis that are critical to effectively treat pathogenic lung infections and inflammatory respiratory diseases.

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Necroptosis in pulmonary macrophages promotes silica-induced inflammation and interstitial fibrosis in mice

Cited by 10 publications

References 32 publications

Enterococcus faecalis -Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis

Enterococcus faecalis -Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis

Unraveling the mechanism of tetrandrine combined with Buyang Huanwu Decoction against silicosis using network pharmacology and molecular docking analyses

Cell type‐specific molecular mechanisms and implications of necroptosis in inflammatory respiratory diseases

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