ArticleCell research2010
S100A8/A9 induces autophagy and apoptosis via ROS-mediated cross-talk between mitochondria and lysosomes that involves BNIP3.
Article in Cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
What it found
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The trial behind it
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Who cites it
139 citing papers in PubMed, 276 citations in OpenAlex.
- Trial
- Modeling stimulus-induced stress responses in microglia-like cells using a commercial iPSC-dCas9-KRAB line.Stem cell research · 2026Article
- S100A9 lactylation facilitated sepsis-related acute respiratory distress syndrome via promoting transcription activation of IL-1β in macrophages.Cell communication and signaling : CCS · 2026Article
- Elucidating the therapeutic efficacy and mechanisms of arctigenin in ameliorating renal fibrosis: a combined transcriptomic and proteomic study.Frontiers in pharmacology · 2026Article
- S100A9 Integrates Autophagic Deficiency With Immunopathology and Latanoprost Responsiveness in Primary Open-Angle Glaucoma.International journal of genomics · 2026Article
- The role of microglia in neurodegenerative diseases: from the perspective of ferroptosis.Acta pharmacologica Sinica · 2025Review
- Mechanism of action and therapeutic potential of S100A8/A9 in neuroinflammation and cognitive impairment: From molecular target to clinical application (Review).International journal of molecular medicine · 2025Review
- Relationship of S100 Proteins with Neuroinflammation.Biomolecules · 2025Review
- Endogenous interactomes of MFN1 and MFN2 provide novel insights into interorganelle communication and autophagy.Autophagy · 2025Article
- Identification and verification of methylenetetrahydrofolate dehydrogenase 1-like protein as the binding target of natural product pseudolaric acid A.Natural products and bioprospecting · 2025Article
- An integrative multiparametric approach stratifies putative distinct phenotypes of blast phase chronic myelomonocytic leukemia.Cell reports. Medicine · 2025Article
- Evaluation of transcriptomic changes after photobiomodulation in spinal cord injury.Scientific reports · 2025Article
- S100A8-CAMKK2-AMPK axis confers the protective effects of mild hypothermia against cerebral ischemia-reperfusion injury in rats.Scientific reports · 2025Article
- The alarmin tandem: unraveling the complex effect of S100A8/A9 - from atherosclerosis to cardiac arrhythmias.Frontiers in immunology · 2025Review
- Extracellular Cold-Inducible RNA-Binding Protein and Hemorrhagic Shock: Mechanisms and Therapeutics.Biomedicines · 2024Review
- Integrated omics profiling reveals systemic dysregulation and potential biomarkers in the blood of patients with neuromyelitis optica spectrum disorders.Journal of translational medicine · 2024Article
- PGAM5 interacts with and maintains BNIP3 to license cancer-associated muscle wasting.Autophagy · 2024Article
- Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction.Current issues in molecular biology · 2024Review
- Analysis of the aging-related biomarker in a nonhuman primate model using multilayer omics.BMC genomics · 2024Article
- Machine learning-based identification of a cell death-related signature associated with prognosis and immune infiltration in glioma.Journal of cellular and molecular medicine · 2024Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
Abstract
The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosis-inducing activity in various cells of different origins. Here, we present evidence that the underlying molecular mechanisms involve both programmed cell death I (PCD I, apoptosis) and PCD II (autophagy)-like death. Treatment of cells with S100A8/A9 caused the increase of Beclin-1 expression as well as Atg12-Atg5 formation. S100A8/A9-induced cell death was partially inhibited by the specific PI3-kinase class III inhibitor, 3-methyladenine (3-MA), and by the vacuole H(+)-ATPase inhibitor, bafilomycin-A1 (Baf-A1). S100A8/A9 provoked the translocation of BNIP3, a BH3 only pro-apoptotic Bcl2 family member, to mitochondria. Consistent with this finding, DeltaTM-BNIP3 overexpression partially inhibited S100A8/A9-induced cell death, decreased reactive oxygen species (ROS) generation, and partially protected against the decrease in mitochondrial transmembrane potential in S100A8/A9-treated cells. In addition, either DeltaTM-BNIP3 overexpression or N-acetyl-L-cysteine co-treatment decreased lysosomal activation in cells treated with S100A8/A9. Our data indicate that S100A8/A9-promoted cell death occurs through the cross-talk of mitochondria and lysosomes via ROS and the process involves BNIP3.
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What 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.