ArticleJournal of cellular and molecular medicine2024
HBSP inhibits tubular cell pyroptosis and apoptosis, promotes macrophage M2 polarization, and protects LPS-induced acute kidney injury.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Pancreatic stone protein inhibits pyroptosis of pancreatic acinar cells in sepsis-associated pancreatic injury.Frontiers in medicine · 2025Article
- Inflammation preservation strategy: reconciling pain control and disc resorption in lumbar disc herniation.Frontiers in immunology · 2025Review
- HBSP inhibits tubular cell pyroptosis and apoptosis, promotes macrophage M2 polarization, and protects LPS-induced acute kidney injury.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
11 authors.
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Abstract
Sepsis-associated acute kidney injury (AKI) has high morbidity and mortality, but without cause-specific treatment. Erythropoietin derived Helix B surface peptide (HBSP) alleviates AKI, whereas its underlying mechanisms remain to be further explored. Here, the effects of HBSP on pyroptosis, apoptosis, macrophage polarization and repair were investigated in lipopolysaccharide (LPS)-induced AKI mouse model and cultured kidney epithelial cells. Systemic inflammation, compromised renal function and histology were demonstrated in LPS-treated mice, with upregulated pyroptotic and apoptotic key proteins in the kidneys including GSDMD-N, cleaved IL-1β, IL-18 and caspase-3. These proteins were localized in tubular areas and colocalized with aquaporin-1 (AQP1), with increased F4/80
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