Overexpression of CD14, TLR4, and MD-2 in HEK 293T cells does not prevent induction of in vitro endotoxin tolerance [PDF]
Andrei E. Medvedev, Stefanie N. Vogel
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From Genome to Geroscience: How DNA Damage Shapes Systemic Decline
Persistent DNA damage triggers systemic secretory responses including damage‐associated molecular patterns (DAMPs), the senescence‐associated secretory phenotype (SASP), and extracellular vesicles (EVs). This non‐cell‐autonomous signaling disrupts intercellular communication, driving organism‐wide dysfunction and aging, and offering new therapeutic ...
Athanasios Siametis, George A. Garinis
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TLR2 and TLR4 bridge physiological and pathological inflammation in the reproductive system. [PDF]
Mansouri A, Akthar I, Miyamoto A.
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TLR4-dependent Lipopolysaccharide-induced Shedding of Tumor Necrosis Factor Receptors in Mouse Bone Marrow Granulocytes [PDF]
Thierry Pédron+2 more
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ABSTRACT Background The ratio of high‐density lipoprotein cholesterol (HDL‐C) to low‐density lipoprotein cholesterol (LDL‐C) predicts cardiovascular disease (CVD) endpoints, yet its prognostic validity in high‐risk populations and for type 2 diabetes mellitus (T2DM)‐related adverse events remains unestablished. Methods This study included 32,609 people
Biting Lin+10 more
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Erratum to“TLR4 Asp299Gly polymorphism is not associated with coronary artery stenosis” [ATH 170 (2003) 187–190] [PDF]
Ian A. Yang, John W. Holloway, Shu Ye
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Abstract Aims Inflammation plays a critical role in both the development and progression of heart failure (HF), which is a leading cause of morbidity and mortality worldwide. However, the causality between specific inflammation‐related proteins and HF risk remains unclear.
Xian‐Guan Zhu+9 more
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Synthesis of Acinetobacter baumannii Lipid A(s) and derivatives and their structure-immunostimulatory activity relationships. [PDF]
Li XR+8 more
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Erratum: Toll-like receptor-4 (TLR4) signaling augments chemokine-induced neutrophil migration by modulating cell surface expression of chemokine receptors [PDF]
Jie Fan, Asrar B. Malik
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