The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
The central role of inflammatory signaling in the pathogenesis of myelodysplastic syndromes
Open accessAbstract
In cancer biology, tumor-promoting inflammation and an inflammatory microenvironment play a vital role in disease pathogenesis. In the past decade, aberrant innate immune activation and proinflammatory signaling within the malignant clone and the bone marrow (BM) microenvironment were identified as key pathogenic drivers of myelodysplastic syndromes (MDS). In particular, S100A9-mediated NOD-like receptor protein 3 (NLRP3) inflammasome activation directs an inflammatory, lytic form of cell death termed pyroptosis that underlies many of the hallmark features of the disease. This circuit and accompanying release of other danger-associated molecular patterns expands BM myeloid-derived suppressor cells, creating a feed-forward process propagating inflammasome activation. Furthermore, somatic gene mutations of varied functional classes license the NLRP3 inflammasome to generate a common phenotype with excess reactive oxygen species generation, Wnt/β-catenin-induced proliferation, cation flux-induced cell swelling, and caspase-1 activation. Recent investigations have shown that activation of the NLRP3 inflammasome complex has more broad-reaching importance, particularly as a possible disease-specific biomarker for MDS, and, mechanistically, as a driver of cardiovascular morbidity/mortality in individuals with age-related, clonal hematopoiesis. Recognition of the mechanistic role of aberrant innate immune activation in MDS provides a new perspective for therapeutic development that could usher in a novel class of disease-modifying agents.
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“Secreted S100 proteins cause autocrine activation and expansion of MDSCs via binding of CD33/Siglec-3.75”
From Inflammatory bone marrow microenvironment (2019) · cites this paper as [75]
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Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS
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Metadata
- Authors
- Sallman, D. A., & List, A.
- Affiliations
- Moffitt Cancer Center (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2019-03-07
- Volume
- 133
- Issue
- 10
- Pages
- 1039-1048
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC7022316
- OpenAlex
- W2913296480
- Cited by
- 273
- References
- 81
- Citations by year
- 2026: 26 · 2025: 27 · 2024: 39 · 2023: 47 · 2022: 38 · 2021: 59 · 2020: 23 · 2019: 14
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P30CA076292)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Hematology › Blood disorders and treatments
- Keywords
- myelodysplastic syndrome, NLRP3 inflammasome, S100A9, pyroptosis, bone marrow microenvironment, myeloid-derived suppressor cells, innate immune activation, clonal hematopoiesis, cardiovascular morbidity, caspase-1, reactive oxygen species, Wnt/β-catenin signaling, disease biomarkers, disease-modifying therapy
- MeSH terms
- Pyroptosis, NLR Family, Pyrin Domain-Containing 3 Protein, Bone Marrow, Bone Marrow Cells, Hematopoiesis, Humans, Immunity, Innate, Inflammation, Mutation, Myelodysplastic Syndromes, Phenotype, Signal Transduction, Reactive Oxygen Species, Inflammasomes
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