BAY61‑3606 attenuates neuroinflammation and neurofunctional damage by inhibiting microglial Mincle/Syk signaling response after traumatic brain injury

He, Xuejun; Huang, Yimin; Liu, Yanchao; Zhang, Xincheng; Yue, Pengjie; Ma, Xiaopeng; Zhang, Miao; Long, Xiaohong; Yang, Yiping; Wan, Xin; Shu, Kai; Lei, Ting; Gan, Chao; Zhang, Huaqiu

doi:10.3892/ijmm.2021.5060

Cited by 23 publications

(18 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CLRs have previously been found to be expressed on neuron membranes [77]. Recently, research demonstrated that the amount of C-type lectin-like receptors was remarkably changed post-TBI [78]. Another recent study on TBI patients indicated that the amount of CLR is intimately associated with TBI severity.…”

Section: Discussionmentioning

confidence: 98%

Role of statins in regulating molecular pathways following traumatic brain injury: A system pharmacology study

Mahmoudi

Heydari

Markina

et al. 2022

Biomedicine & Pharmacotherapy

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 98%

Role of statins in regulating molecular pathways following traumatic brain injury: A system pharmacology study

Mahmoudi

Heydari

Markina

et al. 2022

Biomedicine & Pharmacotherapy

View full text Add to dashboard Cite

“…CLRs’ dysregulation results in the production of inflammatory mediators and the development of inflammatory diseases following excessive injury. Microglial macrophage-inducible C-type lectin (Mincle), a critical member in CLRs, widely expressed on antigen-presenting cells (APCs), including macrophages, binds nuclear spliceosome-Associated Protein 130 (SAP130) from necrotic cells to enhance neuroinflammation (Del Fresno et al, 2020 ; He et al, 2022 ). After the injury, Mincle and its activated downstream spleen tyrosine kinase (Syk) boost inflammatory gene expression levels in alcohol-induced liver injury mice (Kim et al, 2018 ).…”

Section: Potential Therapeutic Targets and Strategies Of Microglia-in...mentioning

confidence: 99%

“…Furthermore, many investigations have suggested that inhibiting the Mincle/Syk signal axis exerts a neuroprotective role associated with various brain diseases in preclinical research. Different intervention treatments, including Syk inhibitor BAY61-3606, acupuncture, and MSCs engraftment, have been used to attenuate microglia-mediated neuroinflammation by impeding Mincle/Syk signaling pathway in microglia following hemorrhage stroke, ischemic stroke, and traumatic brain injury (TBI; He et al, 2015 , 2022 ; de Rivero Vaccari et al, 2015 ; Liu X. Y. et al, 2018 ; Li Y. et al, 2021 ). According to the above analysis, the Mincle/Syk signaling pathway can be utilized as a promising therapeutical target in ICH.…”

Section: Potential Therapeutic Targets and Strategies Of Microglia-in...mentioning

confidence: 99%

Neuroinflammation of microglia polarization in intracerebral hemorrhage and its potential targets for intervention

Yang

Fan

Mazhar

et al. 2022

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Microglia are the resident immune cells of the central nervous system (CNS) and play a key role in neurological diseases, including intracerebral hemorrhage (ICH). Microglia are activated to acquire either pro-inflammatory or anti-inflammatory phenotypes. After the onset of ICH, pro-inflammatory mediators produced by microglia at the early stages serve as a crucial character in neuroinflammation. Conversely, switching the microglial shift to an anti-inflammatory phenotype could alleviate inflammatory response and incite recovery. This review will elucidate the dynamic profiles of microglia phenotypes and their available shift following ICH. This study can facilitate an understanding of the self-regulatory functions of the immune system involving the shift of microglia phenotypes in ICH. Moreover, suggestions for future preclinical and clinical research and potential intervention strategies are discussed.

show abstract

“…Additionally, Mincle is a C-type lectin receptor whose activation has been shown in vitro to promote the release of pro-inflammatory cytokines and pyroptosis of macrophages ( Gong et al, 2020 ). Inhibition of the Mincle/Syk/NF-κB signaling pathway can also reduce the expression of ASC and caspase-1 ( He et al, 2022 ). Although there is still a lack of research on the role of CLRs and TLRs in pyroptosis of DN, their effects on pyroptosis in other cells should not be ignored.…”

Section: Three Molecular Mechanisms Of Pyroptosismentioning

confidence: 99%

NLRP3-mediated pyroptosis in diabetic nephropathy

Wan

Pan

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Diabetic nephropathy (DN) is the main cause of end-stage renal disease (ESRD), which is characterized by a series of abnormal changes such as glomerulosclerosis, podocyte loss, renal tubular atrophy and excessive deposition of extracellular matrix. Simultaneously, the occurrence of inflammatory reaction can promote the aggravation of DN-induced kidney injury. The most important processes in the canonical inflammasome pathway are inflammasome activation and membrane pore formation mediated by gasdermin family. Converging studies shows that pyroptosis can occur in renal intrinsic cells and participate in the development of DN, and its activation mechanism involves a variety of signaling pathways. Meanwhile, the activation of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome can not only lead to the occurrence of inflammatory response, but also induce pyroptosis. In addition, a number of drugs targeting pyroptosis-associated proteins have been shown to have potential for treating DN. Consequently, the pathogenesis of pyroptosis and several possible activation pathways of NLRP3 inflammasome were reviewed, and the potential drugs used to treat pyroptosis in DN were summarized in this review. Although relevant studies are still not thorough and comprehensive, these findings still have certain reference value for the understanding, treatment and prognosis of DN.

show abstract

BAY61‑3606 attenuates neuroinflammation and neurofunctional damage by inhibiting microglial Mincle/Syk signaling response after traumatic brain injury

Cited by 23 publications

References 54 publications

Role of statins in regulating molecular pathways following traumatic brain injury: A system pharmacology study

Role of statins in regulating molecular pathways following traumatic brain injury: A system pharmacology study

Neuroinflammation of microglia polarization in intracerebral hemorrhage and its potential targets for intervention

NLRP3-mediated pyroptosis in diabetic nephropathy

Contact Info

Product

Resources

About