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This research investigates the role of p300-mediated histone acetylation in promoting kidney disease in sickle cell disease patients.

December 8, 2025BloodOpen Access

Targeting p300-mediated histone acetylation inhibits neutrophilic proteinase 3 and prevents the development of sickle chronic kidney disease

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Findings show p300 inhibition reduces neutrophilic PR3, improving renal health in sickle cell patients with CKD.

This research investigates the role of p300-mediated histone acetylation in promoting kidney disease in sickle cell disease patients.
Examined the impact of heme-induced activation of neutrophils on EPCR cleavage in sickle mice.
Utilized flow cytometry and RNA sequencing to analyze neutrophil activity and gene expression in renal tissues.
Administered garcinol to inhibit p300 and assess its effect on CKD development in sickle mice.
Heme challenge elevated PR3 levels in renal neutrophils, contributing to CKD pathogenesis.
Garcinol treatment significantly reduced PR3 expression and preserved EPCR levels in SS mice kidneys.
Histological and biochemical evaluations confirmed the protective effects of garcinol against CKD development.

Pant et al. (2025) studied this question.

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