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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Authors

RPRajat PantIndian Institute of Technology Roorkee PMParitosh MondalUniversity of Pittsburgh DLDiane LenhartUniversity of Pittsburgh

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Implication

Targeting heme-induced neutrophilic proteinase pr3 suppresses CKD progression in sickle cell disease, highlighting a potential intervention for kidney protection.

Key Points

Neutrophilic proteinase-3 accumulation in kidneys is associated with chronic kidney disease in sickle cell disease.
Efficacy of the p300 inhibitor garcinol shows significant reduction of pr3 expression and enhances EPCR levels.
Transcriptomic analysis reveals heme-induced pathways linking neutrophil activation to kidney damage mechanisms.
The findings suggest promising directions for novel therapies targeting neutrophil-mediated injury in sickle chronic kidney disease.

Cite This Study

Pant et al. (2025) studied this question.

synapsesocial.com/papers/69362f744fa91c937236e33b https://doi.org/10.1182/blood-2025-840

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Implication

Targeting heme-induced neutrophilic proteinase pr3 suppresses CKD progression in sickle cell disease, highlighting a potential intervention for kidney protection.

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

Discussion

Member takes

Implication

Key Points

Cite This Study

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

Discussion

Member takes

Implication

Key Points

Cite This Study

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