Atrial cardiomyocyte-restricted cleavage of gasdermin D promotes atrial arrhythmogenesis.

ABSTRACT:

Background and aims

Enhanced inflammatory signalling causally contributes to atrial fibrillation (AF) development. Gasdermin D (GSDMD) is an important downstream effector of several inflammasome pathways. However, the role of GSDMD, particularly the cleaved N-terminal (NT)-GSDMD, in non-immune cells remains elusive. This study aimed to elucidate the function of NT-GSDMD in atrial cardiomyocytes (ACMs) and determine its contribution to atrial arrhythmogenesis.

Methods

Human atrial appendages were used to assess the protein levels and localization. A modified adeno-associated virus 9 was employed to establish ACM-restricted overexpression of NT-GSDMD in mice.

Results

The cleavage of GSDMD was enhanced in ACMs of AF patients. Atrial cardiomyocyte-restricted overexpressio

SUBMITTER: Yuan Y 

PROVIDER: S-EPMC11959185 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature