Targeting the NLRP3 inflammasome abrogates cardiotoxicity of immune checkpoint blockers.

ABSTRACT:

Background

Immune checkpoint inhibitors (ICIs) have revolutionized the treatment of many malignant tumors. However, ICI-induced hyper-immune activation causes cardiotoxicity. Traditional treatments such as glucocorticoids and immunosuppressants have limited effectiveness and may even accelerate tumor growth. This study aimed to identify approaches that effectively reduce cardiotoxicity and simultaneously preserve or enhance the antitumor immunity of ICI therapy.

Methods

ICI injection in melanoma-bearing C57BL/6J female mice was used to simulate cardiotoxicity in patients with tumor undergoing immune therapy. MCC950 was used to block nod-like receptor protein 3 (NLRP3) inflammasome activity. Echocardiography, immunofluorescence, flow cytometry, and reverse transcription quant

SUBMITTER: Lu Y 

PROVIDER: S-EPMC11749606 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature