AI Article Synopsis
- * In patients with sepsis, EPCs in peripheral blood undergo pyroptosis, a form of programmed cell death, though the underlying mechanism is not fully understood.
- * The study identified that high levels of serum HMGB1 from inflammatory macrophages trigger pyroptosis in EPCs via its interaction with the RAGE receptor, suggesting a critical pathway in this process.
Article Abstract
Endothelial dysfunction is an important factor in the progress of sepsis. Endothelial progenitor cells (EPCs) are the precursor cells of endothelial cells and play a crucial role in the prognosis and treatment of sepsis. EPCs in the peripheral blood of patients with sepsis undergo pyroptosis, but the mechanism remains much of unknown. Serum high-mobility group box-1 (HMGB1) is significantly elevated in patients with sepsis, but whether it is related to EPCs pyroptosis is unknown. We used a cell model of sepsis to isolate EPCs for better observation. By detecting the pyroptosis-related indicators of EPCs and the level of release and acetylation of HMGB1 in inflammatory macrophages, it was found that HMGB1 released by inflammatory macrophages combined with receptor for advanced glycation end products (RAGE) is a key pathway to induce pyroptosis of EPCs.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11483297 | PMC |
| http://dx.doi.org/10.1016/j.isci.2024.110996 | DOI Listing |
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