ArticleBritish journal of pharmacology2015
Toll-interacting protein contributes to mortality following myocardial infarction through promoting inflammation and apoptosis.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- NLRP3 Regulation in Neonatal Hypoxic-Ischemic Encephalopathy-Focus on Microglial Activation.International journal of molecular sciences · 2026Article
- Fibroblast-Derived Microfibrillar-Associated Protein 5 Exerts Cardioprotective Effects After Myocardial Infarction by Activating the NOTCH2 Signaling in Cardiomyocytes.Journal of the American Heart Association · 2026Article
- From mitochondria to heart: the role and challenges of mitochondrial antiviral signaling protein in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- RING finger protein 5 protects against acute myocardial infarction by inhibiting ASK1.BMC cardiovascular disorders · 2024Article
- Anshen Shumai Decoction inhibits post-infarction inflammation and myocardial remodeling through suppression of the p38 MAPK/c-FOS/EGR1 pathway.Journal of molecular histology · 2024Article
- Meteorin‑like/meteorin‑β protects against cardiac dysfunction after myocardial infarction in mice by inhibiting autophagy.Experimental and therapeutic medicine · 2024Article
- Regulation of Key Immune-Related Genes in the Heart Following Burn Injury.Journal of personalized medicine · 2022Article
- Peiminine inhibits myocardial injury and fibrosis after myocardial infarction in rats by regulating mitogen-activated protein kinase pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Role of miRNA-324-5p-Modified Adipose-Derived Stem Cells in Post-Myocardial Infarction Repair.International journal of stem cells · 2021Article
- MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- Overexpression of TOLLIP Protects against Acute Kidney Injury after Paraquat Intoxication through Inhibiting NLRP3 Inflammasome Activation Modulated by Toll-Like Receptor 2/4 Signaling.Mediators of inflammation · 2021Article
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- LncRNA-GAS5 regulates PDCD4 expression and mediates myocardial infarction-induced cardiomyocytes apoptosis via targeting MiR-21.Cell cycle (Georgetown, Tex.) · 2020Article
- lncRNA-ZFAS1 induces mitochondria-mediated apoptosis by causing cytosolic CaCell death & disease · 2019Article
- Regulation mechanism of aquaporin 9 gene on inflammatory response and cardiac function in rats with myocardial infarction through extracellular signal-regulated kinase1/2 pathway.Heart and vessels · 2019Article
- Pretreatment with Total Flavonoid Extract from Dracocephalum Moldavica L. Attenuates Ischemia Reperfusion-induced Apoptosis.Scientific reports · 2018Article
- Tollip Negatively Regulates Vascular Smooth Muscle Cell-Mediated Neointima Formation by Suppressing Akt-Dependent Signaling.Journal of the American Heart Association · 2018Article
- Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway.PloS one · 2018Article
- New targets to alleviate skeletal muscle inflammation: role of microRNAs regulated by adiponectin.Scientific reports · 2017Article
- Aging and Autophagy in the Heart.Circulation research · 2016Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeToll-interacting protein (Tollip) is an endogenous inhibitor of toll-like receptors, a superfamily that plays a pivotal role in various pathological conditions, including myocardial infarction (MI). However, the exact role of Tollip in MI remains unknown. EXPERIMENTAL APPROACH: MI models were established in Tollip knockout (KO) mice, mice with cardiac-specific overexpression of human Tollip gene and in their Tollip(+/+) and non-transgenic controls respectively. The effects of Tollip on MI were evaluated by mortality, infarct size and cardiac function. Hypoxia-induced cardiomyocyte damage was investigated in vitro to confirm the role of Tollip in heart damage. KEY
resultsTollip expression was dramatically up-regulated in human ischaemic hearts and infarcted mice hearts. MI-induced mortality, infarct size and cardiac dysfunction were decreased in Tollip-KO mice compared with Tollip(+/+) controls. Ischaemic hearts from Tollip-KO mice exhibited decreased inflammatory cell infiltration and reduced NF-κB activation. Tollip depletion also alleviated myocardial apoptosis by down-regulating pro-apoptotic protein levels and up-regulating anti-apoptotic protein expressions in infarct border zone. Conversely, MI effects were exacerbated in mice with cardiac-specific Tollip overexpression. This aggravated MI injury by Tollip in vivo was confirmed with in vitro assays. Inhibition of Akt signalling was associated with the detrimental effects of Tollip on MI injury; activation of Akt largely reversed the deleterious effects of Tollip on MI-induced cardiomyocyte death. CONCLUSIONS AND IMPLICATIONS: Tollip promotes inflammatory and apoptotic responses after MI, leading to increased mortality and aggravated cardiac dysfunction. These findings suggest that Tollip may serve as a novel therapeutic target for the treatment of MI.
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