ArticleCell death & disease2014
Caspase-dependent cell death-associated release of nucleosome and damage-associated molecular patterns.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
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- A role for TNF-α in alveolar macrophage damage-associated molecular pattern release.JCI insight · 2020Article
- Molecular mechanisms of biogenesis of apoptotic exosome-like vesicles and their roles as damage-associated molecular patterns.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Expanding the genetic code of Mus musculus.Nature communications · 2017Article
- An Early and Robust Activation of Caspases Heads Cells for a Regulated Form of Necrotic-like Cell Death.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis, which is anti-inflammatory, and necrosis, which is pro-inflammatory, represent the extremes of the cell death spectrum. Cell death is complex and both apoptosis and necrosis can be observed in the same cells or tissues. Here, we introduce a novel combined mode of cellular demise--caspase-dependent regulated necrosis. Most importantly, it is mainly characterized with release of marked amount of oligo- or poly-nucleosomes and their attached damage-associated molecular patterns (DAMPs) and initiated by caspase activation. Caspase-activated DNase has dual roles in nucleosomal release as it can degrade extracellularly released chromatin into poly- or oligo-nucleosomes although it prohibits release of nucleosomes. In addition, osmotically triggered water movement following Cl(-) influx and subsequent Na(+) influx appears to be the major driving force for nucleosomal and DAMPs release. Finally, Ca(2+)-activated cysteine protease, calpain, is an another essential factor in nucleosomal and DAMPs release because of complete reversion to apoptotic morphology from necrotic one and blockade of nucleosomal and DAMPs release by its inhibition.
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