Toll‐interacting protein contributes to mortality following myocardial infarction through promoting inflammation and apoptosis
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Summary
Toll‐interacting protein is an endogenous inhibitor of toll‐like receptors, a superfamily that plays a pivotal role in various pathological conditions, including myocardial infarction, but the exact role of Tollip in MI remains unknown.
- Type
- article
- Published
- 2015-07-01
- Cited by
- 26
- References
- 54
- Access
- Open access
- OpenAlex
- https://openalex.org/W1596610401
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:41796752
Keywords
Protein kinase B, Apoptosis, Inflammation, Biology, Transgene
References
- Tollip, a new component of the IL-1RI pathway, links IRAK to the IL-1 receptor
- The Concise Guide to Pharmacology 2013/14: Enzymes
- Cooperation of Toll-Like Receptor 2 and 6 for Cellular Activation by Soluble Tuberculosis Factor and Borrelia burgdorferi Outer Surface Protein A Lipoprotein: Role of Toll-Interacting Protein and IL-1 Receptor Signaling Molecules in Toll-Like Receptor 2 Signaling1
- THE CONCISE GUIDE TO PHARMACOLOGY 2013/14: CATALYTIC RECEPTORS
- C1q/TNF-Related Protein-9, a Novel Adipocyte-Derived Cytokine, Attenuates Adverse Remodeling in the Ischemic Mouse Heart via PKA Activation
- The IUPHAR/BPS Guide to PHARMACOLOGY: an expert-driven knowledgebase of drug targets and their ligands
- Neutrophil depletion reduces myocardial apoptosis and attenuates NFkappaB activation/TNFalpha release after ischemia and reperfusion.
- Inhibition of p53 after acute myocardial infarction: reduction of apoptosis is counteracted by disturbed scar formation and cardiac rupture.
- Tollip attenuated the hypertrophic response of cardiomyocytes induced by IL-1beta.
- Apoptosis and post-infarction left ventricular remodeling.
- Neutrophils—A Key Component of Ischemia-Reperfusion Injury
- A mechanistic role for cardiac myocyte apoptosis in heart failure.
- Interferon Regulatory Factor 1 Is Required for Cardiac Remodeling in Response to Pressure Overload
- Signal Regulatory Protein-α Protects Against Cardiac Hypertrophy Via the Disruption of Toll-Like Receptor 4 Signaling
- Deficiency of Capn4 Gene Inhibits Nuclear Factor-κB (NF-κB) Protein Signaling/Inflammation and Reduces Remodeling after Myocardial Infarction*
- Epigallocatechin-3-gallate-mediated Tollip induction through the 67-kDa laminin receptor negatively regulating TLR4 signaling in endothelial cells.
- PPAR-γ AND TOLLIP ARE ASSOCIATED WITH TOLL-LIKE RECEPTORS IN COLITIS RATS
- Regulation of cardiac hypertrophy by intracellular signalling pathways
- Tumor necrosis factor receptor‐associated factor 5 is an essential mediator of ischemic brain infarction
- Interferon regulatory factor 9 is an essential mediator of heart dysfunction and cell death following myocardial ischemia/reperfusion injury
Cited by
- Interferon Regulatory Factor Signalings in Cardiometabolic Diseases
- Aging and Autophagy in the Heart
- New targets to alleviate skeletal muscle inflammation: role of microRNAs regulated by adiponectin
- Reprogramming Innate Immune Signaling in Cardiometabolic Disease
- Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway
- Circulating Long Noncoding RNA HOTAIR is an Essential Mediator of Acute Myocardial Infarction
- Tollip Negatively Regulates Vascular Smooth Muscle Cell–Mediated Neointima Formation by Suppressing Akt‐Dependent Signaling
- Pretreatment with Total Flavonoid Extract from Dracocephalum Moldavica L. Attenuates Ischemia Reperfusion-induced Apoptosis
- Integrated Omics Reveals Tollip as an Regulator and Therapeutic Target for Hepatic Ischemia‐Reperfusion Injury in Mice
- Regulation mechanism of aquaporin 9 gene on inflammatory response and cardiac function in rats with myocardial infarction through extracellular signal-regulated kinase1/2 pathway
- lncRNA-ZFAS1 induces mitochondria-mediated apoptosis by causing cytosolic Ca2+ overload in myocardial infarction mice model
- LncRNA-GAS5 regulates PDCD4 expression and mediates myocardial infarction-induced cardiomyocytes apoptosis via targeting MiR-21
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease
- MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3
- Isorhynchophylline ameliorates paraquat-induced acute kidney injury by attenuating oxidative stress and mitochondrial damage via regulating toll-interacting expression.
- Role of miRNA-324-5p-Modified Adipose-Derived Stem Cells in Post-Myocardial Infarction Repair
- Overexpression of TOLLIP Protects against Acute Kidney Injury after Paraquat Intoxication through Inhibiting NLRP3 Inflammasome Activation Modulated by Toll-Like Receptor 2/4 Signaling
- Peiminine inhibits myocardial injury and fibrosis after myocardial infarction in rats by regulating mitogen-activated protein kinase pathway
- Regulation of Key Immune-Related Genes in the Heart Following Burn Injury
- Anshen Shumai Decoction inhibits post-infarction inflammation and myocardial remodeling through suppression of the p38 MAPK/c-FOS/EGR1 pathway
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