2021
DOI: 10.1177/0300060521997590
|View full text |Cite
|
Sign up to set email alerts
|

Role of TLR4/MyD88/NF-κB signaling in heart and liver-related complications in a rat model of type 2 diabetes mellitus

Abstract: Aims To analyze expression of members of the Toll-like receptor (TLR)4/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling pathway in the heart and liver in a rat model of type 2 diabetes mellitus (T2DM). Our overall goal was to understand the underlying pathophysiological mechanisms. Methods We measured fasting blood glucose (FBG) and insulin (FINS) in a rat model of T2DM. Expression of members of the TLR4/MyD88/NF-κB signaling pathway as well as downstream cytokines was inves… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
2

Citation Types

1
12
0

Year Published

2021
2021
2024
2024

Publication Types

Select...
10

Relationship

0
10

Authors

Journals

citations
Cited by 23 publications
(13 citation statements)
references
References 37 publications
1
12
0
Order By: Relevance
“…Lipopolysaccharide (LPS) in the blood circulation forms a complex with CD14 of monocyte macrophages, which is recognized by toll-like receptor 4 (TLR4) on the surface of immune cells. They could activate nuclear transcription factors through myeloid differentiation molecule 88 (MyD88) [ 3 ] and promote the synthesis and secretion of many inflammatory factors including tumor necrosis factor α, interferon γ, and interleukin-6, which may further affect the insulin resistance and T2DM [ 4 ].…”
Section: Introductionmentioning
confidence: 99%
“…Lipopolysaccharide (LPS) in the blood circulation forms a complex with CD14 of monocyte macrophages, which is recognized by toll-like receptor 4 (TLR4) on the surface of immune cells. They could activate nuclear transcription factors through myeloid differentiation molecule 88 (MyD88) [ 3 ] and promote the synthesis and secretion of many inflammatory factors including tumor necrosis factor α, interferon γ, and interleukin-6, which may further affect the insulin resistance and T2DM [ 4 ].…”
Section: Introductionmentioning
confidence: 99%
“…In response to activated TLR4/NF-κB, proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 were markedly triggered concomitant to reduced antiinflammatory cytokines such as IL-10 in mice with T2DM, implying the key role of inflammatory events in the pathophysiology of myocardial injury. 65 The findings of the study revealed that BCP treatment significantly reduced the expression levels of TLR4, p-NF-κB p65, and p-IκBα, revealing prevention of TLR4/NF-κB signaling.…”
Section: ■ Discussionmentioning
confidence: 82%
“…As a highly conserved pattern recognition receptor, it can interact with endogenous ligands such as Heat shock protein(HSP), fibrinogen, High Mobility Group Box 1 protein(HMGB1), Oxidized low density lipoprotein(OX-LDL) and exogenous ligands such as LPS released by Gram-negative bacteria [ 27 29 ]. The activation of Nuclear factor-kappa B(NF-κB) was induced by regulating the dependent or independent signaling pathways of Myeloid differentiation factor 88(MyD88) [ 30 ]. TLR4/MyD88/NF-κB signaling pathway leads to the increase of downstream pro-inflammatory cytokines and adhesion molecules, participate in the occurrence of inflammatory reactions [ 31 ], and cause the pathological changes such as vascular extravasation or increased vascular permeability, vascular obstruction, and degeneration and pathological changes of neovascularization, thus leading to the occurrence and development of DMI [ 32 , 33 ].…”
Section: Discussionmentioning
confidence: 99%