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Peer-reviewedCC BY 4.0Frontiers in Immunology

Monocyte-macrophage sensing of calciprotein particles in CKD-associated vascular calcification: lysosomal stress and inflammasome activation

  • Zhiqiang Xu1
  • Yuying Jiang2
  • Kangwei Wang1
  • Zehao Jin1,3
  1. 1The Affiliated Yueqing Hospital, Wenzhou Medical University
  2. 2Taizhou Central Hospital (Taizhou University Hospital)
  3. 3Technical University of Munich
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Abstract

Chronic kidney disease (CKD) exposes the circulation to sustained calcium-phosphate stress. Calciprotein particles (CPPs) buffer mineral supersaturation and, alongside mineral and bone disorder, uremic toxins, oxidative stress, and inflammation, are an important potential contributor to vascular injury. This mini-review examines how monocytes and macrophages recognize and process CPPs, with emphasis on lysosomal stress and inflammatory responses. Scavenger receptor A contributes to the uptake of mature CPPs in experimental models. In human monocytes studied under high-calcium conditions relevant to rheumatoid arthritis, the calcium-sensing receptor enhances macropinocytosis and CPP uptake. Subsequent responses vary with particle preparation, dose, cell type, and priming. Reported effects include altered lysosomal acidification and proteolysis, and membrane damage in selected models. Genetic and pharmacological studies support the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome and the release of caspase-1-dependent interleukin-1β. Interleukin-1α release and necrotic injury can persist independently of this pathway. Separate vascular studies have reported endothelial dysfunction and smooth muscle cell calcification after CPP exposure, but have not established that myeloid CPP sensing mediates these effects in CKD. Particle heterogeneity and non-equivalent assays limit the ability to make comparisons across studies. Interventions that reduce mineral loading or delay CPP maturation affect some particle-related measures, but their effects on clinical vascular outcomes remain uncertain.

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Cite

BibTeXRIS
BibTeX
@article{xu2026monocytemacrophage,
  title = {{Monocyte-macrophage sensing of calciprotein particles in CKD-associated vascular calcification: lysosomal stress and inflammasome activation}},
  author = {Zhiqiang Xu and Yuying Jiang and Kangwei Wang and Zehao Jin},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1982842},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1982842/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Monocyte-macrophage sensing of calciprotein particles in CKD-associated vascular calcification: lysosomal stress and inflammasome activation
AU  - Zhiqiang Xu
AU  - Yuying Jiang
AU  - Kangwei Wang
AU  - Zehao Jin
PY  - 2026
DA  - 2026/10/23
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1982842
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1982842/full
AB  - Chronic kidney disease (CKD) exposes the circulation to sustained calcium-phosphate stress. Calciprotein particles (CPPs) buffer mineral supersaturation and, alongside mineral and bone disorder, uremic toxins, oxidative stress, and inflammation, are an important potential contributor to vascular injury. This mini-review examines how monocytes and macrophages recognize and process CPPs, with emphasis on lysosomal stress and inflammatory responses. Scavenger receptor A contributes to the uptake of mature CPPs in experimental models. In human monocytes studied under high-calcium conditions relevant to rheumatoid arthritis, the calcium-sensing receptor enhances macropinocytosis and CPP uptake. Subsequent responses vary with particle preparation, dose, cell type, and priming. Reported effects include altered lysosomal acidification and proteolysis, and membrane damage in selected models. Genetic and pharmacological studies support the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome and the release of caspase-1-dependent interleukin-1β. Interleukin-1α release and necrotic injury can persist independently of this pathway. Separate vascular studies have reported endothelial dysfunction and smooth muscle cell calcification after CPP exposure, but have not established that myeloid CPP sensing mediates these effects in CKD. Particle heterogeneity and non-equivalent assays limit the ability to make comparisons across studies. Interventions that reduce mineral loading or delay CPP maturation affect some particle-related measures, but their effects on clinical vascular outcomes remain uncertain.
SN  - 1664-3224
ER  -