S100a9 inhibits Atg9a transcription and participates in suppression of autophagy in cardiomyocytes induced by β₁-adrenoceptor autoantibodies.

ABSTRACT:

Background

Cardiomyocyte death induced by autophagy inhibition is an important cause of cardiac dysfunction. In-depth exploration of its mechanism may help to improve cardiac dysfunction. In our previous study, we found that β₁-adrenergic receptor autoantibodies (β₁-AAs) induced a decrease in myocardial autophagy and caused cardiomyocyte death, thus resulting in cardiac dysfunction. Through tandem mass tag (TMT)-based quantitative proteomics, autophagy-related S100a9 protein was found to be significantly upregulated in the myocardial tissue of actively immunized mice. However, whether S100a9 affects the cardiac function in the presence of β₁-AAs through autophagy and the specific mechanism are currently unclear.

Methods

In this study, the act

SUBMITTER: Zhi X 

PROVIDER: S-EPMC10506287 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature