The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure

Yu, Lili; Feng, Zhiwei

doi:10.1155/2018/9874109

Cited by 117 publications

(116 citation statements)

References 121 publications

(137 reference statements)

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“…Toll-like receptors (TLRs) belong to PRRs, and they are crucial in host protection against microbial infections as they generate innate immune response (Vidya et al, 2017). They recognize both PAMPs and DAMPs derived from tissue damage (Yu & Feng, 2018;Gauthier et al, 2010). The ligands for TLR are extremely broad, ranging from hydrophilic nucleic acids to hydrophobic lipids and from small-sized compounds to macromolecules (Wang et al, 2015).…”

Section: Pattern Recognition Receptors (Prrs)mentioning

confidence: 99%

“…To date, 10 human and 13 murine subtypes of TLR have been identified, although TLR10 is non-functional in the mouse (Wang et al, 2015). They can recognize both the external pathogen-associated molecular patterns (PAMPs) (Zhang & Liang, 2016) and the internal damage-associated molecular patterns (DAMPs) (Yu & Feng, 2018). They are expressed on all innate immune cells such as macrophage, neutrophils, dendritic cells (DCs), natural killer (NK) cells, mast cells, basophils, and eosinophil (Delneste et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Toll-like receptors activation, signaling, and targeting: an overview

2019

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Background: Toll-like receptors (TLRs) are an important family of receptors that constitute the first line of defense system against microbes. They can recognize both invading pathogens and endogenous danger molecules released from dying cells and damaged tissues and play a key role in linking innate and adaptive immunity. TLRs are widely distributed in both immune and other body cells. The expressions and locations of TLRs are regulated in response to specific molecules derived from pathogens or damaged host cells. The binding of ligands to TLR activates specific intracellular signaling cascades that initiate host defense reactions. Such binding is liganddependent and cell type-dependent and leads to production of pro-inflammatory cytokines and type 1 interferon. TLR-dependent signaling pathways are tightly increased during innate immune responses by a variety of negative regulators. Overactivation of TLRs can ultimately lead to disruption of immune homeostasis and thus increase the risk for inflammatory diseases and autoimmune disorders. Antagonists/inhibitors targeting the TLR signaling pathways have emerged as novel therapeutics to treat these diseases. Aim of work: The present review summarizes the structure, characterizations, and signaling of TLRs and their regulators, as well as describes the implication of TLRs in many diseases with a brief idea about the inhibitors that target TLR signaling pathways. Conclusion: We conclude that TLRs are the main elements of our immune system, and they should be maintained functioning to keep the integrity of innate immunity. Targeting of TLR signaling represents a new challenge for treatment of many diseases.

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Section: Pattern Recognition Receptors (Prrs)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Toll-like receptors activation, signaling, and targeting: an overview

2019

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“…TLRs belong to type I transmembrane glycoproteins with 20-27 leucine-rich repeat motifs for ligand recognition at N-terminus, a single transmembrane helix and a conserved cytoplasmic Toll/Interleukin-1 (IL-1) receptor (TIR) domain at C-terminus for intracellular signaling transduction (Bryant et al 2015). They can functionally recognize external pathogen-associated molecular patterns (PAMPs) and internal damage-associated molecular patterns (DAMPs) (Yu and Feng 2018). While external ligands include lipopeptides, lipopolysccharides (LPS), and bacterial flagellin (Ayres and Schneider 2012), internal ligands include hyaluronan, fibrinogen, heat shock proteins, and elements of damaged/fragmented DNA and RNA ( Fig.…”

Section: Overview Of Toll-like Receptorsmentioning

confidence: 99%

Micronutrients and many important factors that affect the physiological functions of toll-like receptors

2019

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Background: Toll-like receptors (TLRs) are type I integral transmembrane receptors involved in recognition and conveying of pathogens to the immune system. These receptors are located either on cell surfaces or within endosomes. They are activated by specific ligand leading to the release of cytokines via signal transduction pathway. The excess production of these cytokines leads to disrupt the immune homeostasis. There are several factors regulating TLR expression and consequently affecting their functions. Among these are inflammation, cytokines, some cellular process, air pollution, depression, stress, some drugs, genetic polymorphism, nutrition, and micronutrients. Some micronutrients (vitamins and trace elements) may be considered as important TLR regulators, as they have immunomodulatory functions. Vitamins D, B12, and A; zinc; copper; and iron have important role on innate immune responses. Aim of work: This review gives a brief idea on TLR family and attempts to cover the factors affecting the physiological functions of them. Conclusion: Of many factors affecting TLRs functions are micronutrients. There is a shortage of researches concerning the effect of micronutrients deficiency on the function of TLRs, all of which focused on vitamin D but other vitamins have not got the same importance that they deserve. This orients our efforts to work at this point in the future.

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“…Heart failure is a chronic inflammatory injury disease of the myocardium. Immune inflammation greatly contributes to the pathogenesis of heart failure , Yu & Feng 2018. During this process, many cytokines and inflammatory molecules are expressed and released, such as TNF-α, IL-1β and IL-6, adhesion molecules and CRP (Torre-Amione et al 2000, Alonso-Martínez et al 2002, Deten et al 2003.…”

Section: Heart Failurementioning

confidence: 99%

Urotensin II: an inflammatory cytokine

Sun

Liu²

2019

Journal of Endocrinology

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Urotensin II (UII) is a polypeptide molecule with neurohormone-like activity. It has been confirmed that UII is widely distributed in numerous organs of different animal species from fish to mammals, including humans. The UII receptor is orphan G-protein-coupled receptor 14, also known as UT. The tissue distribution of UII and UT is highly consistent, and their expression may be regulated by autocrine and paracrine mechanisms. In the body, UII has many physiological and pathophysiological activities, such as vasoconstrictor and vasodilatory actions, cell proliferation, pro-fibrosis, neuroendocrine activity, insulin resistance and carcinogenic and inflammatory effects, which have been recognized only in recent years. In fact, UII is involved in the process of inflammatory injury and plays a key role in the onset and development of inflammatory diseases. In this paper, we will review the roles UII plays in inflammatory diseases.

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The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure

Cited by 117 publications

References 121 publications

Toll-like receptors activation, signaling, and targeting: an overview

Toll-like receptors activation, signaling, and targeting: an overview

Micronutrients and many important factors that affect the physiological functions of toll-like receptors

Urotensin II: an inflammatory cytokine

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