Interaction between non-coding RNAs and Toll-like receptors

Ghafouri‐Fard, Soudeh; Abak, Atefe; Shoorei, Hamed; Talebi, Seyedeh Fahimeh; Mohaqiq, Mahdi; Sarabi, Parisa; Taheri, Mohammad; Mokhtari, Majid

doi:10.1016/j.biopha.2021.111784

Cited by 16 publications

(14 citation statements)

References 127 publications

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“…Its activation results in the induction of the NF-κB pathway and the production of inflammatory cytokines, contributing to the innate immune system (Ghafouri-Fard et al. 2021 ). As a critical inflammatory regulator, TLR4 can activate NF-κB and IRF3 through the MyD88-dependent pathway and the TRIF-dependent pathway in I/R cardiac, stimulating the expression of pro-inflammatory and immunoregulatory cytokine genes and mediating cascade inflammation (Ramalingam et al.…”

Section: Discussionmentioning

confidence: 99%

Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway

Chen

et al. 2022

Pharmaceutical Biology

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Context Acacetin is a natural source of flavonoids with anti-inflammatory and antioxidant effects. Objective This study determines acacetin’s protective effect and mechanism on myocardial ischaemia/reperfusion (I/R) injury. Materials and methods Sprague-Dawley rats were divided into sham and I/R injury and treatment with acacetin. Acacetin (10 mg/kg) was subcutaneously injected for 7 days. ECG and echocardiography were conducted to determine arrhythmia and heart function. The pathological characters of the heart were determined with triphenyl tetrazolium chloride staining, Haematoxylin & Eosin staining, and Masson staining. Expression of proteins in infarct tissues was examined with western blots. Results Administrated with acacetin in I/R rats significantly reduced the arrhythmia score from 4.90 to 2.50 and the reperfusion arrhythmia score from 3.79 to 1.82 in the vehicle or the acacetin group, respectively. LVEF was improved from 33.5% in the I/R group to 43.7% in the acacetin group, LVFS was increased from 16.4% to 24.5%, LVIDs was decreased from 6.5 to 5.3 mm. The inflammatory cell infiltration, myocardial fibrosis, and collagen 1 and 3 were reduced by acacetin. Acacetin promoted SOD and decreased MDA. In myocardial tissues, the expression level of TLR4 and IL-6 were restrained, and IL-10 was promoted. Apoptotic protein Bax was suppressed, and anti-apoptotic protein Bcl-2 was promoted in the acacetin group. Interestingly, the transcription factor Nrf-2/HO-1 pathway was also reversed by acacetin. Discussion and conclusion Our findings indicated that acacetin has a potential therapeutic effect in clinical application on treating I/R-induced heart injury.

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Section: Discussionmentioning

confidence: 99%

Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway

Chen

et al. 2022

Pharmaceutical Biology

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“…These may include infectious, autoimmune/inflammatory, or neoplastic diseases. Recently, ( Ghafouri-Fard et al, 2021a ), have unveiled the interaction between ncRNAs and Toll-like receptors (TLRs) in transducing both MyD88-dependent and TRIF-dependent signaling cascades to induce human inflammatory and autoimmune disorders. Furthermore, the same group have found in the literature that both miRs and lncRNAs can regulate bone development processes including osteogenesis.…”

Section: Pathogenesis Of Osteoporosis and Osteogenesis In As Patientsmentioning

confidence: 99%

The Potential Role of Genetics, Environmental Factors, and Gut Dysbiosis in the Aberrant Non-Coding RNA Expression to Mediate Inflammation and Osteoclastogenic/Osteogenic Differentiation in Ankylosing Spondylitis

Liao

Tsai

Lai

et al. 2022

Front. Cell Dev. Biol.

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Ankylosing spondylitis (AS) or radiographic axial spondyloarthritis is a chronic immune-mediated rheumatic disorder characterized by the inflammation in the axial skeleton, peripheral joints, and soft tissues (enthesis, fascia, and ligament). In addition, the extra-skeletal complications including anterior uveitis, interstitial lung diseases and aortitis are found. The pathogenesis of AS implicates an intricate interaction among HLA (HLA-B27) and non-HLA loci [endoplasmic reticulum aminopeptidase 1 (ERAP1), and interleukin-23 receptor (IL23R), gut dysbiosis, immune plasticity, and numerous environmental factors (infections, heavy metals, stress, cigarette smoking, etc.) The latter multiple non-genetic factors may exert a powerful stress on epigenetic regulations. These epigenetic regulations of gene expression contain DNA methylation/demethylation, histone modifications and aberrant non-coding RNAs (ncRNAs) expression, leading to inflammation and immune dysfunctions. In the present review, we shall discuss these contributory factors that are involved in AS pathogenesis, especially the aberrant ncRNA expression and its effects on the proinflammatory cytokine productions (TNF-α, IL-17 and IL-23), T cell skewing to Th1/Th17, and osteoclastogenic/osteogenic differentiation. Finally, some potential investigatory approaches are raised for solving the puzzles in AS pathogenesis.

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“…The virus triggers a lot of co‐receptors able to start signals, which, in turn, activate several immunological mechanisms: genetic, epigenetic, pre‐existing immunity, polymorphisms of signals/receptors of the immune system, and actually may contribute to the heterogeneity of the final response. Table 2 compares the receptors targeted by S1 protein for their structure, cell, and tissue distribution, and pathophysiology, 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 , 101 whereas Figure 2 summarizes the pathways of each receptor and the antigenic activity of S1 influencing the immune response.…”

Section: Immuno‐pathogenesis Of Covid‐19mentioning

confidence: 99%

What we know and still ignore on COVID‐19 immune pathogenesis and a proposal based on the experience of allergic disorders

Maggi

Azzarone

Canonica

et al. 2021

Allergy

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The coronavirus disease 2019 (COVID‐19) pandemic started in March 2020 and caused over 5 million confirmed deaths worldwide as far August 2021. We have been recently overwhelmed by a wide literature on how the immune system recognizes severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and contributes to COVID‐19 pathogenesis. Although originally considered a respiratory viral disease, COVID‐19 is now recognized as a far more complex, multi‐organ‐, immuno‐mediated‐, and mostly heterogeneous disorder. Though efficient innate and adaptive immunity may control infection, when the patient fails to mount an adequate immune response at the start, or in advanced disease, a high innate‐induced inflammation can lead to different clinical outcomes through heterogeneous compensatory mechanisms. The variability of viral load and persistence, the genetic alterations of virus‐driven receptors/signaling pathways and the plasticity of innate and adaptive responses may all account for the extreme heterogeneity of pathogenesis and clinical patterns. As recently applied to some inflammatory disorders as asthma, rhinosinusitis with polyposis, and atopic dermatitis, herein we suggest defining different endo‐types and the related phenotypes along COVID‐19. Patients should be stratified for evolving symptoms and tightly monitored for surrogate biomarkers of innate and adaptive immunity. This would allow to preventively identify each endo‐type (and its related phenotype) and to treat patients precisely with agents targeting pathogenic mechanisms.

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Interaction between non-coding RNAs and Toll-like receptors

Cited by 16 publications

References 127 publications

Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway

Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway

The Potential Role of Genetics, Environmental Factors, and Gut Dysbiosis in the Aberrant Non-Coding RNA Expression to Mediate Inflammation and Osteoclastogenic/Osteogenic Differentiation in Ankylosing Spondylitis

What we know and still ignore on COVID‐19 immune pathogenesis and a proposal based on the experience of allergic disorders

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