ArticleInternational journal of clinical and experimental pathology2017
High-mobility group Box-1 regulates acute myocardial ischemia-induced injury through the toll-like receptor 4-related pathway.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Isoproterenol induces MD2 activation by β-AR-cAMP-PKA-ROS signalling axis in cardiomyocytes and macrophages drives inflammatory heart failure.Acta pharmacologica Sinica · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
High-mobility group box-1 (HMGB1) is a nuclear protein released by necrotic cells as a result of its interactions with several receptors, including the receptor for advanced glycation end-products (RAGE) and members of the toll-like receptor family. HMGB1 has been implicated in autoimmune diseases and hepatic and intestinal ischemia/reperfusion (I/R) injury; however, its role in myocardial ischemia-induced injury remains unclear. In this study, isoproterenol (ISO) was used to establish a myocardial ischemia mouse model. Treating mice with recombinant HMGB1 (rHMGB1) worsened myocardial injury, whereas treating mice with antibodies that neutralized HMGB1 significantly reduced tissue damage. Interestingly, myocardial ischemia severity was not affected by rHMGB1 or HMGB1 antibody administration in toll-like receptor 4 (TLR4)-deficient mice (TLR4-/-), which demonstrated significantly reduced ischemia-induced cardiac tissue damage compared with wild-type (WT) mice. HMGB1 plays an important role in myocardial ischemia-induced injury by binding to TLR4, which results in proinflammatory pathway activation and enhanced myocardial injury. Therefore, blocking HMGB1 or TLR4 may represent a novel therapeutic strategy for treating myocardial ischemia-induced injury.
Indexed as
Identifiers
31966685PMC6965424W3028572188What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.