ArticleMolecules and cells2025
Pentraxin 3 deficiency ameliorates streptozotocin-induced pancreatic toxicity via regulating ER stress and β-cell apoptosis.
Article in Molecules and cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Differential Anti-Inflammatory Effects of Semaglutide and Tirzepatide in Experimental Diabetes Mellitus.Current issues in molecular biology · 2026Article
- Molecules and Cells 2025, highlights from molecules to organisms.Molecules and cells · 2026Article
- Pharmacological chaperones mitigate noise-induced hearing loss by attenuating sustained PERK activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Electroacupuncture mitigates Bacillus Calmette-Guérin (BCG)-induced depression-like behavior and neuroinflammation via BDNF and NF-κB pathway in mice.Animal cells and systems · 2026Article
- Boosting the engraftment of subcutaneously transplanted pancreatic islets by nanofat.Diabetes, obesity & metabolism · 2025Article
- Reciprocal rescue of Wolfram syndrome by two causative genes.EMBO reports · 2025Article
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Authors and funding
5 authors.
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Abstract
The long pentraxin 3 (PTX3), a marker of inflammation, has been associated with cardiovascular disease, obesity, and metabolic syndrome. Recently, elevated serum PTX3 levels have been linked to type 2 diabetes in obese patients with nonalcoholic fatty liver disease. Diabetes mellitus is a metabolic syndrome characterized by hyperglycemia resulting from insufficient insulin secretion or action. However, the precise role of PTX3 in hyperglycemia remains unclear. This study aimed to investigate the physiological roles of PTX3 in vivo. The deformation of pancreatic islets was mitigated in PTX3-deficient mice treated with streptozotocin (STZ) compared to control C57BL/6J mice. In addition, PTX3 deficiency prevented STZ-induced unfolded protein responses and pancreatic β-cell death. Immunoblotting data revealed significant inhibition of inositol-requiring protein1α and C/EBP homologous protein (CHOP) protein expression in PTX3 KO mice administered tunicamycin which is a chemical endoplasmic reticulum stress inducer. Similarly, tunicamycin-induced Grp78, Grp94, ATF6, and CHOP mRNA levels were reduced in PTX3 KO mice. Moreover, recombinant PTX3-induced CHOP expression and β-cell apoptosis in primary mouse islets. These findings suggest that PTX3 plays a critical role in STZ-induced deformation of pancreatic islets via regulating endoplasmic reticulum stress and β-cell apoptosis.
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